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The Chicken Health Handbook 

■ his must-have reference for the small flock owner covers the 
problems and diseases common to chickens of all breeds and all 
ages. Generously illustrated, The Chicken Health Handbook 
teaches you how to: 

V hatch healthy chicks 

V provide proper nutrition 

V fight parasites 

V spot diseases and infections in their early stages 

V protect flocks from predators 

V build safe houses and yards 

,. . ;« T/,p Chicken Health Handbook help pin- 
toe syndrome. 

.4 first-rale guide . . . Planless. 

- American Library Association 


ISBN 978-0-88266-611-2 



If you don't have any books on chickens, this 
is the only one you need. If you ha ve a book- 
shelf full of books, you still need this one. 

- Poultry Press 

A small-scale farmer in Tennessee, Gail 
Damerow has written numerous articles on rais- 
ing chickens. She is the editor of Rural Heritage 
magazine and the author of sev en hooks, includ- 
ing Chickens in Your Backyard, Ducks and Geese 
in Your Backyard, and Your Chickens: A Kid's 
Guide to Raising and Showing. 

Storey Publishing 

S19.95 US 


Gail Damerow 

Storey Publishing 


The mission of Storey Publishing is to serve our customers by 

publishing practical information that encourages 
personal independence in harmony with the environment. 

Edited by Amanda R. Haar 
Cover design by Meredith Maker- 
Text design and production by Cynthia McFarland 
Cover photograph ©John Col-well from Grant Heilmann Photography 
Line drawings by Elayne Sears except chapter opene; 

art on pages 6 and 216 by Cynthia McFarland 
Indexed by Gail Damero-w 

©1994 by Gail Damerow 

All rights reserved. No part of this book may be reproduced without written per- 
mission from the publisher, except by a reviewer who may quote brief passages or 
reproduce illustrations in a review with appropriate credits; nor may any part of 
this book be reproduced, stored in a retrieval system, or transmitted in any form 
or by any means — electronic, mechanical, photocopying, recording, or other 
— without written permission from the publisher. 

The information in this book is true and complete to the best of our knowledge. 
All recommendations are made without guarantee on the part of the author or 
Storey Publishing. The author and publisher disclaim any liability in connection 
with the use of this information. For additional information, please contact Storey 
Publishing, 210 MASS MoCA Way, North Adams, MA 01247. 

Storey books are available for special premium and promotional uses and for 
customized editions. For further information, please call 1-800-793-9396. 

Printed In the United States by Versa Press 
JO 29 28 

Library of Congress Cataloging-in-Publication Data 

Damerow, Gail. 

Chicken health handbook / Gail Damerow 
p. cm. 

Includes bibliographical references (p. ) and index. 
ISBN 978-0-88266-611-2 (pbk.) 

1. Chickens — Diseases. 2. Chickens — Health. 3i Chickens — Parasites, t. Title. 
SW9S.D33 1994 

636.5-089— dc20 93-33385 



Charts v 

Foreword by Jeanne Smith, D.V.M vii 

Introduction 1 

Chicken Health 3 

Health and Nutrition 26 

Anatomy of a Chicken 43 

External Parasites 58 

Internal Parasites: Worms 77 

Internal Parasites: Protozoa 97 

Infectious Diseases 107 

Enviromnent-Related Problems 132 

I . Diagnostic Guides 1 47 

10. Postmortem Examination 165 

Therapy 181 

Enhancing Immunity 197 

Incubation and Brooding 208 

Chickens and Human Health 230 

Diseases and Disorders 244 

Glossary 315 

Suppliers 324 

State Poultry Pathology Laboratories 325 

Recommended Reading 331 

Index 333 


1-1 Diseases Spread by Carriers 8 

1- 2 Minimum Space Requirements 15 

1 -3 Survival Ability of Disease-Causing Organisms 18 

1 -4 Chemical Disinfectants 20 


2- 1 Vitamin Benefits and Sources 30 

2-2 Nutritional Diseases and Disorders 33 

2-3 Nutritional Symptoms 34 

2-4 Feeding Schedule ■ • • 36 

2-5 Feeder Space 37 

2-6 Restricted Feeding Schedule for Pullets 38 

2-7 Diseases Affecting Water Consumption 39 

2-8 Diseases Related to Drinking Water 39 

2-9 Environmental Temperature and Water Consumption 40 

2-10 Signs of Water Deprivation 41 

2- 11 Waterer Space and Minimum Water Needs 41 


3- 1 Diseases Involving the Cloacal Bursa 45 

3-2 Air Sacs 48 

3- 3 Disorders by the Body System They Affect 56 


4- 2 Lice 65 

4-3 Mites 68 

4- 4 Chiggers 



5- 2 Tapeworms 90 

5- 3 Flukes 



6- 1 Protozoan Diseases 97 

6-2 Coccidia Affecting Chickens 100 

6-3 Drugs Used to Treat Coccidiosis 103 


7-1 Bacterial Diseases ■ .........4-1 110 

7-2 Viruses Infecting Chickens 120 

7-3 Forms of Newcastle Disease 125 

7-4 Forms of Marek's Disease 1^1 

7-5 Differences Between Lymphoid Leukosis and Marek's Disease 1 28 

7- 6 Fungal Diseases 130 


8- 1 Fungal Poisoning 141 

8-2 Toxic Plants 142 

8-3 Rodent Droppings 143 

8-4 Rodenticides 146 

9-1 Flock History 148 

9-2 Signs of Health 148 

9-3 Diseases Causing a Change in Droppings 152 

9-4 Diseases Interfering with Movement 154 

9-5 Diseases and Conditions Affecting Egg Production 156 

9-6 Diseases Causing Breathing Difficulties . • ■ 158 

9-7 Diseases Causing Discoloration 159 

9-8 Diseases Causing Off Odors 160 

9-9 Diseases Affecting the Eyes 161 

9-10 Diseases Causing Sores in theMoudi 162 

9-11 Diseases Causing Temperature Changes 162 

9-12 Diseases Causing a High Rate of Death 163 

9-13 Diseases Causing Sudden Death 164 

Chapter 10 

10-1 Postmortem Findings 174 

10-2 Inflamed Conditions 179 

10- 3 Nutritionally Related Findings 180 

Chapter 11 THERAPY 

11- 1 Reportable Diseases 196 


12- 1 Vaccination Mediods 205 


13- 1 Nutrition-Related Hatching Problems 217 

13-2 Incubation Trouble-Shooting 218 

13- 3 Nutritional Problems in Chicks 228 

CnmenU chickens and human health 

14- 1 Poultry-Related Human Diseases 231 

14-2 Food- Borne Bacteria 238 

14-3 Bacterial Food Poisoning Quick-Check 240 


IN MY VETERINARY PRACTICE 1 work with many poultry fanciers and backyard 
poultry farmers. I am often asked what books I could recommend to help them 
learn better management and gain a better understanding of the diseases that 
may affect their birds. I bave been unable to help them much with dieir requests, 
as most of the texts on avian diseases are written for veterinarians, of limited use- 
fulness to the layperson. Very few books are available for the fancier, and those 
that I have seen are generally incomplete and not particularly accurate. 

Therefore, 1 am delighted to see this publication being made available to the 
poultry fancier. Gail Damerow has covered the topic of small-flock poultry health 
management very completely and competently. The information is presented 
accurately and in enough detail to give the fancier a full understanding of the dis- 
eases, their prevention and treatments. Yet this is done in an easily understood 
manner through careful attention to definitions and explanations. It is not an easy 
task to convert scientific information that veterinarians study for years to under- 
stand into useful, management-bottom-line information for the average back- 
yard poultry grower. I believe Ms. Damerow has accomplished this in her book. 

Ms. Damerow has also presented her information in a quite accessible format 
for the fancier. She not only describes each disorder as a distinct entity, wliich can 
be looked up by the fancier who has just received a diagnosis and wants to learn 
more about the disease, but she also has provided a section arranged by clinical 
signs. The fancier, seeing certain clinical signs in the flock, can go to the book and 
look up what the possible causes are. Both of these approaches will have their 
usefulness for the fancier. 

Prevention of disease through good management is essential when raising 
poultry, especially small flocks of poultry, which are often not vaccinated for many 
of the diseases that commercial poultry are, which often travel to and from shows, 
and which are maintained in multi-age facilities. Also, the generally low monetary 
value of individual birds makes costs of diagnosis and treatments impractical in 
many cases. Having a book such as this which outlines good disease prevention 
strategies, as well as disease management strategies should problems occur, is a 
valuable asset to the poultry' fancier. 

I believe the best use of this book is to read it through for the disease preven- 
tion management information whether you are having disease problems in your 
birds or not. Implement whatever management practices you are not already us- 
ing. Then keep the book handy as a reference if you see a problem pop up in your 

Jeanne Smith, D.V.M. 
Avian Health Services 
3220 Quail Drive, Placerville, CA 95667 



THIS BOOK WAS BORN out of years of frustration in trying to deal with 
chicken diseases and not being able lo find a clearly understandable, in-depth 
source of information. Books that ate easy to understand are usually not com- 
plete — often failing to contain the very information needed most. On the 
other hand, comprehensive books rarely make sense to the non-specialist. 
Making matters worse, most printed information is geared toward operators of 
large commercial flocks, who deal with quite a different set of problems from 
those experienced by small-flock owners. 

Since I couldn't find the book I needed, after years of experience raising 
chickens I decided to write it. I've tried to include all the information necessary 
to keep a small Hock healthy, while avoiding technical details that have no 
practical application (do you really need to know which bacteria are gram- 
negative, polar-staining, and non-motile?). 

ens might experience, but I've covered all the common problems and many 
less common ones you'll likely never see but will surely be interested in, if one 
of them turns up in your flock. 

Years ago, when I was secretary of the Pacific Poultry Breeders Association 
and was responsible for putting out the organization's newsletter, I was ac- 
cused of placing too much emphasis on diseases. Complainers grumbled that 
chicken-keepers (especially novices) might get the idea that raising chickens 
involves a constant battle with diseases. 

Those complaints haunted me as I wrote this book, so I wish to make clear 
that my aim is not to discourage you from keeping chickens. It is, rather, to 

to increase your disease awareness so you can recognize any problem that 
might occur and take action before the problem gets out of hand. 

How you approach injury or disease in your flock depends a great deal on 
your purpose in keeping chickens, whedier it is to enjoy healthful meat and 
eggs, to have fun showing your birds, or to make money selling homegrown 
meat or eggs. This book provides information pertaining to all three situations. 
It is not for the commercial grower who takes an impersonal view of individual 


2 The Chicken Health Handbook 

3, who medi- 
cates them to the max, and who breeds for ever-greater growth or production 
at the expense of disease resistance. (Diseases found primarily in commercial 
flocks are described here, however, so you can watch out for them if you live in 
a major poultry-producing area.) 

I wish to thank Randy Holliman of Hoechst-Roussel Agri-Vet Company in 
Murfreesboro, Tennessee, for helping me learn how to do a home fecal test; L. 
Dwight Schwartz, D.V.M., avian health consultant with Avicon, Inc. in 
Okemos, Michigan, for reviewing my chapter on "Diseases and Disorders" and 
helping fill in the gaps; Arthur A. Bickford, D.V.M., of the California Veterinary 
Laboratory in Turlock for his thorough review and numerous helpful sugges- 
tions; and Jeanne Smith, D.V.M., of Avian Health Services in Placerville, 
California, for her technical review and wonderful insights into the problems 
of small-flock ownership. 

Chicken Health 

DURING THE PAST CENTURY, most of the serious diseases that once plagued 
poultry keepers have been brought under control. It wasn't that long ago, for 
example, that we discovered viruses and invented vaccines against them, or 
that we first began to understand the life cycles of internal parasites and were 
finally able to control them. 

While we have been busy learning to control old diseases, new ones have 
appeared. Some were always there, to be discovered as technology improved. 
Others have popped up out of the blue. Still others have been caused by the 
way modem poultry flocks are managed. So, while technology gives us new 
ways to fight diseases, it also gives us new diseases to fight. 

What Is Disease? 

Disease is defined as a departure from health and includes any condition that 
impairs normal body functions. Disease results from a combination of indirect 
causes (called "stress") that reduce resistance and direct causes that produce 
the disease. 

Direct causes of disease can be divided into two categories: infectious and 
non-infectious. Infectious diseases result from invasion of the body by another 
living organism — bacteria, viruses, fungi, protozoa, and a variety of internal 
and external parasites. Non-infectious diseases are caused by nutritional 
problems (deficiency or excess), chemical poisons, traumatic injury, or even 
excessive stress. 


4 The Chicken Health Handbook 

Fresh air and 
promote good 

Technically speaking, all infectious diseases are parasitic, and all parasitic 
invasions are infectious. By convention, the word "parasite" is often used to 

identify infectious diseases caused by 





Microorganisms causing infectious 

animal forms, most of which can be 
seen with the naked eye (worms, lice, 
mites, and the like). 

The word "infection" is generally re- 
served for invasion by other forms, 
which all happen to be microscopic 
(bacteria, virus, fungi, etc.). The dis- 
tinction breaks down, however, in the 
case of protozoa, which are both ani- 
mal forms and microscopic. (In this 
book, protozoa are grouped with the 
other animal forms.) 

Regardless of a disease's cause, be- 
fore you can effectively control it, you 
must know how diseases in general are 
introduced and how they spread. 

Reservoirs of Infection 

Diseases are introduced from reservoirs of infection, defined as any source 
or site where a disease-causing organism survives or multiplies and from 
which it can be transferred to a host — in this case, a chicken. A reservoir of 
infection may be animate or inanimate. 

Chicken Health 5 

Animate or living reservoirs include: 

• chickens and other domestic poultry 

• exotic and cage birds 

• wild birds 

• wild animals (including rodents) 

• livestock 

• household pets 

• humans 

• earthworms, snails, and slugs 

• arthropods (fleas, mites, ticks, lice, and mosquitoes t 
crickets, and grasshoppers that chickens eat) 

Some disease-causing organisms, such as the infectious bronchitis virus, 
are species specific for chickens, meaning diey affect only chickens. Others are 
shared among different kinds of poultry, such as the avian reovirus, which in- 
fects bodi chickens mid turkeys. Some microbes are harmless to one type of 
fowl but devastating to others, such as the Marek's disease virus that's com- 
mon and harmless in turkeys but potentially deadly to chickens. Some 
microbes, including Salmonella bacteria, infect a wide variety of vertebrates 
including humans. A few infectious organisms spend part of dieir life cycles 
living in arlhropods that parasitize chickens or that spread disease to chickens 
through their bites. 

A chicken may serve as its own reservoir of infection, as occurs when a 
disease is caused by an organism the chicken normally carries on or in its body. 
Examples are streptococci and Pasteurella bacteria, bodi of which infect a bird 
after its resistance has been reduced by some other cause. Dead chickens, im- 
properly disposed of, can also serve as reservoirs of infection, if their bodies are 
pecked by susceptible chickens. 

Inanimate reservoirs of infection include: 

• feed containing fungi or bacteria 

• water, 
fungi, or protozoa thrive 

• litter, soil, and dust harboring spore-bearing organisms that produce 
disease when they get into a chicken's tissue, often through a wound 

• so-called "fomites" — articles dial can be contaminated by disease- 
causing organisms. Examples of fomites include a crate used for 
carrying chickens, an incubator used for hatching chicks, or a brooder 
in which chicks are raised. A fomite can be either a reservoir of infec- 
tion or merely a vehicle diat serves as a means of spreading infectious 
organisms from one place to another. 

6 The Chicken Health Handbook 

Once a disease has been introduced, il may spread from one chicken lo 
another in two ways: 

eggs (or, in the case of some viruses, from an infected cock through 

semen fertilizing the eggs); 

Direct contact occurs when an infected bird and a susceptible bird peck, 
preen, or mate one another. Diseases that spread through contact widi the 
skin of an infected bird include pox and influenza (caused by viruses) and sta- 
phylococcal and streptococcal infections (caused by opportunistic bacteria). 
Staph and strep infections also spread through direct mucus-to-mucus con- 
tact during mating. 

Indirect contact occurs by means of a vehicle (sometimes called a 
"mechanical vector"). A vehicle is anything, living or otherwise, capable of 
transporting disease-causing organisms from one place to another. Like reser- 
voirs of infection, vehicles can be either animate or inanimate. 



Chicken Health 7 

Animate vehicles include: 

• wild birds, rodents, household pets, and other animals tiiat carry 
infectious organisms on their feet, feathers, or fur (as distinct from 
diseased animals that spread infection through their saliva, droppings, 
or urine); 

• flies and other arthropods that carry disease on their feet or bodies (as 
distinct from infected arthropods that spread disease by injecting 
contaminated saliva); 

• humans who carry disease-causing organisms on their clothing, shoes, 
skin, or hair, including fanciers who visit one another, vaccination 
crews that travel from place to place, meter readers, electricians, 
plumbers, and feed delivery personnel. 

Inanimate vehicles include: 

• shed skin, feathers, droppings, broken eggs, and other debris from 
infected birds; 

• feed and drinking water contaminated by body discharges from 
infected birds, including undrained puddles and streams that run past 
one flock and then another; 

• air, which wafts dust, fluff, fine bits of dried droppings, and droplets of 
respiratory moisture expelled by breathing, sneezing, or coughing 
(most airborne infections do not spread far); 

flockwide vaccination of infected and susceptible birds alike; 
• used equipment, egg cartons, waterers, feeders, feed sacks, tires (of 
cars, trucks, or wheelbarrows), and other fo mites to which body 
discharges containing disease-causing microbes may cling, to be 
transported for hundreds of miles. 


Many diseases are spread by carriers. A carrier is a bird that does not show 
symptoms of a disease, yet harbors the organism that causes the disease. Car- 
riers may be active or passive. An active carrier once had symptoms of the 
disease but has since recovered. A passive carrier never developed symptoms. 
Whether active or passive, a carrier sheds and spreads disease-causing or- 

Diseases that produce carriers usually are not worth curing. You can cure a 
bird of infectious coryza, for instance, but you have no way of knowing if the 
bird will become a carrier and spread die disease to susceptible birds in the 

8 The Chicken Health Handbook 

isms, and the more likely it is to be a carrier. Since growing and adult birds 
carry levels of microbes that chicks and young birds can't resist, birds of vari- 
ous ages should never be mixed together. 

Diseases Spread by Carriers 




Air-sac disease 























not common 

Chronic respiratory disease 






Infectious bronchitis 



Infectious coryza 



Infectious laryngotracheitis 



Infectious synovitis 


not common 










Lymphoid leukosis 



Marek's disease 






Newcastle (exotic) 





very common 
















Ulcerative enteritis 



Chicken Health 9 


"Biosecurity" is the latest buzzword in the world of poultry health. It means 
protecting your flock from infectious diseases and it encompasses any precau- 
tion you take to prevent diseases from entering or surviving in your yard. 

Different sectors of the poultry industry place emphasis on different 
biosecurity measures. The USDA favors all-in, all-out management, which 
works fine for commercial broiler and layer operations, but not for an ongoing 
backyard flock. Manufacturers of pharmaceuticals promote the use of antibi- 
otics and other drugs as a means of controlling disease, but the use of drugs for 
non-medical purposes has serious drawbacks in commercial and backyard 
flocks alike. 

No single biosecurity measure provides the perfect answer to preventing 
disease. Instead, protect your flock with a well-thought-out program of inter- 
related precautions, thoroughly grounded in old-fashioned common sense. 

As part of your common sense biosecurity program: 

• keep a flock history 

• start with good foundation stock 

• maintain a closed flock 

• breed for resistance 

• medicate only as necessary 

• provide a sound environment 

• practice good sanitation 

• minimize stress 

• feed a balanced ration 

Flock History 

A flock history is basically a diary that includes anything and everything 
pertaining to your flock. Start it the moment you acquire your first birds, not- 
ing the date (or date of hatch — if you purchase by mail, it will be on the 
shipping carton), source, strain (if applicable), anything the seller tells you 
about the birds' past history, and any health certificates that come with the birds. 

Document your feeding and management practices and any changes you 
make, including vaccinations you give and medications you use. Write things 
down as you go along. It may seem like a time-consuming chore, but it's a lot 
easier than trying to reconstruct events later if you need the information to 
help trace a health problem. 

The "Flock History" chart on page 148 lists additional information to in- 
clude in your flock history. 

10 The Chicken Health Handbook 

Foundation Stock 

lis difficult to maintain a healthy flock unless you start out with healthy 
stock. The best way to make sure the birds are healthy is to purchase locally, so 
you can see whether or not they come from a healthful environment. You can 
then ask the seller, eye to eye, about the birds' ages and health history, and you 
can see for yourself if any of the seller's birds have symptoms of diseases that 
might be carried by die birds you plan to buy. 

You'll have the least chance of getting diseased birds if you start with newly 
hatched chicks. The older the bird, the more disease problems it has been ex- 
posed to. If you do purchase older birds, take time to check their appearance. 
Make sure they have glossy plumage, look perky and active, and don't show 
any signs of stress behavior. 

Flocks enrolled in the National Poultry Improvement Plan (NP1P) are cer- 
tified to be free of pullorum and typhoid. Some are also free of mycoplasmosis. 
(Information on how to obtain the latest NPIP directory is offered in the ap- 
pendix.) Unfortunately, you may not find an NPIP member who has the kind 
of birds you want. 

Don't buy birds if you are not totally satisfied with their background in 
terms of genetics, management, sanitation, or health history, Above all, avoid 
birds from live-bird auctions, flea markets, wheeler-dealers, traders, 
uncertified hatcheries, and any other source where birds are brought together 
from far-flung flocks. 

Closed Flock 

Each flock is exposed to a unique set of disease-causing organisms, so that 
each develops its own distinct set of immunities. Birds from two healthy 
(locks can therefore give each other diseases for which the others have no 

Once your flock is established, the best way to avoid diseases is to keep a 
closed flock. Keeping a closed flock means avoiding direct or indirect contact 
with other birds. Complete avoidance isn't always possible, but knowing the 
dangers helps keep them to a minimum. 

Maintaining a closed flock means you don't: 

• mix birds from various sources 

• bring in new birds 

• return a bird to your property once it's been elsewhere 

• visit other flocks 

• let owners of other flocks visit yours 


Excluding Wild Birds 

Wild birds are seriously endan- 
gered due to the cutting down 

and other disturbances to their 
natural environment. Instead 
of trapping or poisoning wild 
birds to keep them away from 
your flock, cover your run with 
wire or plastic mesh. If your 

• hatch eggs from other flocks 

• allow wild birds free access to 
your yard 

Unfortunately for biosecurity, Visit- 
ing other flocks is part of the fun of 
having chickens. If you do visit other 
flocks, slip plastic grocery bags over your 
shoes and tie the handles around your 
ankles. When the visit is over, seal the 
two bags in a third bag for disposal. If 
other flock owners visit you, ask them to 
do the same. You may feel foolish wear- 
ing plastic bags on your feet, but you'll 
feel even more foolish if you spread a dis- 
ease to someone else's birds or bring a 
disease home to your flock. 

Trading and showing birds are other 
fun activities that breach biosecurity. Al- 
though diseases are more likely to be spread by trading than by showing, 
occasionally a highly contagious disease (most often infectious laryngo- 
tracheitis) does make the show rounds. To be on the safe side, isolate any 
returning show bird or incoming new bird with two or three sacrificial culls 
from your flock. If your old chickens remain healthy after about a month, 
chances are good the incoming chicken is not a carrier. 

an overhead cover is impracti- 
cal, place their feeders indoors 
so spilled grain won't attract 
wild birds. 

Breeding for Resistance 

Old poultty books make frequent references to "constitutional vigor." The 
concept is quite simple: in every flock some individuals are less affected by 
diseases than others. Susceptible birds get sick or die when exposed to a dis- 
ease. Resistant birds (those with "constitutional vigor") get mildly sick and 
recover quickly or don't get ill at all. 

Developing your flock's genetic resistance means breeding only those 
birds that are less affected by disease, so you'll raise more like them. The re- 
mainder should be culled. In this context, cull means kill — it does not mean 
passing on your problem birds to someone else. 

Some poultry specialists take the position that small -flock owners should 
purchase new stock each year and that raising chicks from your own breeder 
flock only promotes disease. Quite the contrary will be true, if you take care to 

Jeffrey (backyard fancier, retired professor of poultry science, and author of 

12 Thf Chickf.n Health Handbook 

Chicken Diseases) advocates the rigid culling of all snifflers, droopers, feather 
millers, poor eaters, and pale-headed birds to be sure they don't reproduce 
their kind. 

Guidelines on Breeding for Resistance 

Keep a minimum breedingflockof aboutfifty birds, soyou'll have theleeway 
to cull vigorously and still maintain a viable flock. 

Use breeders that are at least two years old, which opposes the conventional 
wisdom that the older the bird, the more diseases it has been exposed to and 

exposure are particularly hearty and may carry maternal antibodies that 
give them further immunity. (Be sure that the disease cannot be egg- 
transmitted from survivor-carriers to their chicks.) 

offspring. Progeny testing requires pedigreeing your birds; in other words, 
you must know exacdy which cock and hen produced each chick (for ideas 
on how to keep track of chicks, see "Chick Identification," page 22 1). For 
progeny testing, Jeffrey suggests this criterion: if the majority of progeny 
from a particular mating live for 1 Vz years, keep the parents in your breeder 
flock; if the majority of progeny do not survive that long, cull die parents and 
the remaining progeny. 

Find indicators or factors known to be related to susceptibility or resistance 
to diseases prevalent in your area. Some indicators can be identified through 
blood typing, a potentially impractical, expensive, and time-consuming 
practice. Other indicators are more accessible to the owner of a small flock. 
For example, resistance to pullorum is associated with a higher than normal 
body temperature in chicks during their first six days of life. 
Give your flock a leg up on resistance by starting with a breed or strain that 
already has some natural resistance to the diseases and parasites they will 
encounter in your area. Leghorns and other light breeds, for example, are 
more resistant to pullorum than Rocks, Reds, and other heavy breeds; Rhod 
Island Reds are more resistant to worms than White Leghorns. 

Breeding for genetic resistance does have its down side: your birds can 
develop resistance only to diseases present in your yard. If a new disease is 
introduced, your chickens may have no defenses against it. Since no tlock can 
be exposed to all possible diseases, no flock can be immune to all possible dis- 
eases. Even if you breed for genetic resistance, you must still take care not to 
introduce new diseases. 

Another aspect to breeding for resistance is that disease-causing organ- 
isms are likely to evolve right along with your resistant strain of birds. These 

Chicken Health 13 

evolving new forms of bacteria and viruses make breeding for resistance a 
never-ending process. 

Medication Schedule 

Using drugs casually, rather than controlling disease through proper man- 
agement, will only increase your problems and your costs. Instead, work out a 
disease prevention program based on the problems prevalent in your area. 
Vaccinate against serious diseases your flock is likely to be exposed to, espe- 
cially epidemic tremor, infectious bronchitis, infectious bursal disease, and 

problem does occur you'll be ready to treat it properly and promptly. 

Sound Environment 

The way you house your chickens influences their state of health. Poultry 
housing falls into four basic categories: 

• cage confinement — common for show birds, pedigreed breeders, and 
large, mechanized laying flocks 

• confinement housing — common for broilers, breeder flocks, and 
floor-managed layers 

• free range — favored for backyard laying flocks and range- fed or so- 
called "organic" meat birds 

• yard and coop — preferred for backyard flocks in the suburbs and 
other areas where space is limited 

Commercial flocks are confined indoors, in cages or on the floor, for sev- 
eral reasons: lighting can be strictly controlled, air can be filtered, and diseases 
that are spread by flying insects and wild birds can be excluded. While con- 
fined flocks are protected from some diseases, as a trade-off diey incur other 
health problems due to lack of sunshine, fresh air, and activity. In addition, if a 

No matter how you choose to house your chickens, they need protection 
from cold, heat, rain, and wind. A sound fence protects them from four-footed 
predators; a covered yard protects them from flying predators. The yard or pen 
should be free of junk and weeds to discourage mice and rats. 

The single most important feature of any chicken house is ease of clean- 
ing. If cleanup is a hassle, you won't do it as often as you ought. The tighter the 

be where pathogens and parasites can hide. 

Smooth surfaces are easier to clean than rough or porous surfaces. Old- 
time poultry keepers used to spray crankcase oil along die bottoms of walls 

14 The Chicken Health Handbook 

and on wood and cement floors, to make these surfaces less penetrable and 
therefore easier to clean. The practice has the additional advantage of control- 
ling roundworms, as well as common insects, but it has the disadvantage of 
creating a fire hazard in wood structures. 

Floors. Flooring can be one of four basic types: 

• A dirt floor is simple and cheap, and it keeps birds cool in warm 
weather. Its disadvantages are that it draws heat in cold weather, does 
not exclude burrowing rodents, and cannot be effectively cleaned. 

• A wood floor invariably has cracks that get packed with tilth, and most 
are built too close to the ground, providing a shallow air space that 
invites invasion by rodents. 

• Droppings boards made of wood battens or welded wire have the 

pick in them Like a wood floor, droppings boards must be placed high 
enough to discourage rodents. 

• Concrete, if well finished, is the most expensive type of flooring, but 
requires minimal repair and upkeep, is easy to clean, and discourages 

Floor Space. Crowded conditions get filthy fast, reduce the flow of fresh air, 
and cause stress — all inducements to disease. The minimum floor space re- 
quirements, including those listed in 
the accompanying chart, may need 
adjustment to suit your specific 
management practices. 

To keep chickens evenly spread 
over the available space, use several 
feeders and waterers and spread them 
around in different locations. In ex- 
tremely cold weather conditions, 
provide heat to prevent huddling. 

Litter management. When chickens 
are kept on a flooring other than drop- 
pings boards, use litter to absorb 
droppings and moisture expelled by 
the flock. For chicks, use 3 inches (7.5 
cm) or more of clean litter that's absor- 
bent, non-toxic, free of mold, and has 
particles too large to be eaten. For adult 
birds, litter should be at least 8 inches 
(20 cm) deep. Dry pine shavings make 


Since droppings tend to accu- 
mulate where chickens perch at 
night, roosts should be placed 
over wooden battens or welded 
wire droppings boards. Allow at 
least 8 inches (20 cm) of roost- 
ing space per bird. Roosts should 
in diameter (1 inch [2.5 cm| for 
bantams) and free of splinters 
and sharp edges that can cause 
foot injuries. To prevent breast 
blisters andbumblefootin broil- 
ers and in cocks of the heavy 
breeds, do not allow these 
heavier birds to roost. 

Chicken Health 15 

Chart 1-2 

Minimum Space Requirements 



Open Housing 

sqfl/Kird Birds/sqm 


sq ft/Bird Birds/sqm 


sq ill/Bird sq cm/Bird 


1 -7 days 





(Do not house 

1 -8 weeks 





heavy breeds 

9-15' weeks 





on wire) 

15-20 weeks 





2 1 weeks + 






1 day-1 week 





1-1 1 weeks 







12-20 weeks 







2 1 weeks + 







Banlams 1 day-1 week 





1-1 1 weeks 







12-20 weeks 







21 weeks + 







*or age of slaughter 

excellent litter. Hardwood shavings, on the other hand, should be avoided due 
to the danger of aspergillosis. 

Remove and replace litter around feeders if it becomes thick with drop- 
pings. Remove and replace moist litter around waterers. Moist litter favors the 
growth of molds (such as those causing aspergillosis) and bacteria (that pro- 
duce ammonia and odier unpleasant gases), and aids the survival of viruses, 
protozoa (such as those causing coccidiosis), and nematodes (worms). 

At least once a year, empty your coop, clean out and replace all the litter, 
and scrape manure from the wails and perches. Fall is the best time for this 
chore, since it puts your flock on clean litter at the start of winter, when bad 
weather keeps chickens indoors much of the time. Compost the used litter or 
spread it on a field where chickens will not range for at least one year. 

If you use the built-up litter system of management (whereby litter is only 
infrequently removed and replaced), compost the litter if you plan to intro- 
duce a replacement flock. The heat produced during composting will destroy 
most pathogens and parasites. 

Ventilation. Fresh air dilutes the population of microbes and reduces the 
buildup of airborne diseases. Good ventilation also keeps air in motion (with- 
out causing draft)' conditions) and removes suspended dust and moisture. 
Moisture tends to be particularly high in a chicken house because chickens 

16 The Chicken Health Handbook 

breathe rapidly, thereby using more air in proportion to their size than any 
other animal. Another important benefit of good ventilation is preventing the 
buildup of ammonia fumes from accumulated droppings. 

Providing an adequate flow of fresh air may require a fan to move out stale 
air and bring in fresh air. Fans are sold according to how many cubic feet of air 
they move per minute (cfm). A good rule of thumb is to get a fan that provides 
5 cfm (.03 cubic meters per minute) per bird. 

Ammonia Check 

I ligh levels of ammonia in the air can reduce feed consumption, affecting the 
growth rate of young birds and the production of laying hens. Ammonia gas 
dissolves in fluid around the eyes, causing irritation, inflammation, and blind- 
ness. Symptoms of ammonia-induced conjunctivitis are rubbing the eye with a 
wing and reluctance to move or go into sunlight. High levels of ammonia can 
also damage the mucous membranes of a bird's respiratory tract, allowing 
bacteria, dust, and viruses to travel down the tract to cause disease. 

Ammonia that is concentrated enough to cause conjunctivitis or respira- 
tory tract damage is concentrated enough to be detected by the human sense of 
smell. To check the ammonia level in your coop, squat or bend down until your 
head is 1 foot (30 cm) above the litter, or about the height of a chicken's head. 
Breathe normally for a moment or two. If your eyes, nose, or throat burn, the 
ammonia level is too high for your birds — decrease litter moisture and improve 
ventilation. Once the condition is corrected, a chicken's cells that were dam- 
aged by ammonia fumes should repair themselves within 2 weeks. 

Chicken Health 17 


After a period of continuous use, chicken housing becomes contaminated 
with disease-causing organisms that may eventually reach infectious levels. 
Regular cleanup does not eliminate microorganisms, but it does keep them at 
bay. You can remove an estimated 95 percent of contamination with a thor- 
ough cleaning. 

Dry cleaning is not nearly as effective as cleaning with water, and hot water 
cleans better than cold water. Detergent (or a 4 percent washing soda solution) 
added to the hot water reduces surface tension and helps the water penetrate 
organic matter. In addition, detergents are mildly germicidal. 

During cleanup, wear a dust mask and avoid inhaling poultry dust, which 
can cause human respiratory problems. Methodically follow these steps: 

• Choose a warm day so facilities will diy quickly. 

• Suppress dust by lightly misting equipment and walls with water and a 
bit of detergent. 

• Remove portable equipment, such as feeders, waterers, nests, and 

• Remove litter and droppings; compost them or spread diem on land 
where your chickens will not range for at least a year. 

• Use a broom, brush, or shop vac to remove dust and cobwebs from the 
ceiling and walls. 

• Brush, blow, or vacuum dust from fans, vents, and any electrical 

• Use a hoe or other scraper to remove manure and dirt clinging to the 
floor, walls, and perches; as long as you can see manure or dirt, keep 

• Turn off electricity and protect electrical equipment and outlets with 
watertight covers or duct tape. 

• Apply detergent or washing soda and hot water systematically to die 
ceiling, walls, floor, and washable equipment with a brush or fruit-tree 
sprayer that delivers 400 psi (pounds per square inch) or 28 kg per sq 
cm for good penetration. 

• Open doors and windows, and turn on the ventilation fan, to air out 
and dry housing before letting the chickens back in. 

• Finish the job by removing any debris that has accumulated around 
the yard since your last cleanup. 


Thoroughly cleaning a chicken house is more important than disinfecting 
it, since many disease-causing organisms cannot survive long in an environ- 

18 Tim Chicken Health Handbook 

Chart 1-3 

Survival Ability of Disease- Causing Organisms 



Survival of Birds 



hours to days 



month or more 







Infectious bronchitis 


week or less 

Infectious bursal disease 



Infectious coryza 


hours to days 

Infectious laryngotracheitis 





days to weeks 

Marek's disease 





hours to days 

Newcastle disease 


month or less 






weeks to months 



months to years 

ment away from birds or their debris. In addition, the microbes that cause 
some diseases — including infectious bursal disease, coccidiosis, and tubercu- 
losis — resist disinfectants. Disinfection, in most cases, should be used only as 
a way to zap stragglers following cleanup. 

Disinfection becomes a necessity if you acquire used equipment or your 
flock experiences an infection. Not aJJ disinfectants work equally well against 
all disease-causing organisms. A veterinarian or poultry pathologist can help 
you select the appropriate disinfectant for your situation. 

Check the date on any disinfectant to be sure it is not outdated. Store the 
disinfectant in a cool place. Some chemicals are quite toxic and should be 
stored away from children, pets, livestock, food, and feeds. To avoid a tragic 
error, keep disinfectants in their original containers with the labels intact. 

Dilute a disinfectant according to either directions on die label or instruc- 
tions provided by a vet or pathologist. Some disinfectants work best in hot 
water, but some evaporate too quickly in warm or hot water. Never mix differ- 
ent kinds of disinfectant, or you may render them all ineffective. Before mixing 
a disinfectant with detergent, lye, washing soda, or other cleaning product, 
check the label for information on compatibility. 

Organic matter inhibits penetradon by a disinfectant, and in some cases 
actually deactivates the disinfectant, so follow the above steps for thorough 
cleanup before applying a disinfectant. If surfaces cannot be scrubbed clean, 

Chicken Health 19 

use a disinfectant that is not readily deactivated by organic matter. Take care, 
though — such disinfectants are quite toxic and should never be applied with a 

Wear goggles to protect your eyes, and avoid inhaling disinfectant chemi- 
cals. After scraping and scrubbing housing clean, close doors and windows 
before applying the disinfectant. Work systematically, starting with the ceiling, 
then the walls, and finally the floor. Afterward, don't forget to disinfect your 
shovel, broom, rake, hoe, and other clean-up tools. Wait at least 20 minutes 
before rinsing equipment and tools to give the disinfectant time to do its job. 

To protect your chickens from skin injury and from respiratory irritation 
due to inhaled chemicals, allow housing to dry thoroughly, and leave the facili- 
ties empty for as long as possible. The safe time between application and 
letting your chickens in varies from 4 hours to 2 days. Consult the label. 

Chem ical Disinfectants 

Chemical disinfectants include: 

Hypochlorites — chlorine-based disinfectants such as chlorine bleach 
(which contains 5 percent available chlorine) and swimming pool chlorine 
(which contains 15 percent). Common brand names are Clorox and Halazone. 
Chlorines work best in warm water but evaporate rapidly, so prepare a fresh 
solution right before use. Chlorine is destructive to fabric, leadter, metal and 
some kinds of plastic. 

Iodine, organic — mixture of iodine with some other chemical. Common 
brand names include Betadine and Isodyne. When the amber color fades, or- 
ganic iodine is no longer effective. 

Quat — quaternary ammonium compound (sometimes also referred to as 
QAC). Quats vary in composition and are widely available at drugstores, pet 
shops, feed stores, and poultry supply outlets. Common brand names include 
Germex and Zephiran. Quats have no strong odor, leave no stains, and are 
non-corrosive, non-irritating, and relatively non-toxic. They cannot be com- 
bined with soap or detergent and will not work on surfaces that are not 
completely free of soap or detergent. 

Phenol — another name for carbolic acid, a coal tar derivative and the 
standard by which all other disinfectants are measured. Common brand 
names include Lysol and Orthophenylphenol. Most chicken keepers consider 
phenols too expensive for use in poultry houses. 

Cresols — coal tar product related to phenol and similar in bactericidal 
properties, once found on every farm. Cresl-400 is one common brand name. 
Cresylic acid is cresol widi soap added. 

Quicklime — also called "slaked lime" is used primarily for damp yards 
where the sun does not shine (and where birds shouldn't be kept, anyway). 

THE Chicki;n Health Handbook 

Chemical Disinfectants 

Iodine Quat Chlorine Cresol Phenol 

Used for: 





Drinking Water 


Effective against: 
Bacterial spores 

Usage level (ppm): 



















Other Properties: 

Toxicity low 

Residual effect no 

Odor little 





Water temperature 








Effective pH 






Deactivated by 

alkaline water 






Deactivated by 

hard water 






Deactivated by 

organic matter 











Apply with spray 






low low high high 

yes no yes yes 

none strong strong strong 

Nonchemical Disinfectants 

Not all disinfectants are chemicals. Here's the rundown on readily avail- 
able nonchemical disinfectants: 

Hot wafer increases the effectiveness of some chemical disinfectants, and 
boiling water and live steam are both effective disinfectants in their own right. 

Chicken Health 21 

Sanitation Terminology 

Products with names ending in "cide" kill the disease-causing agent named in 
the first part: a bactericide kills bacterial cells, a fungicide kills molds and fungi, 
a viricide kills or inactivates viruses, a germicide kills bacteria, but not necessar- 
ily their spores (most germicides are also viricides). 

Products ending in "stat" retard the growth of the organism named in the 
first part: a bacteriostat slows the growth of bacteria, a fungistat slows the 
growth of molds or fungi, and so forth. 

Antiseptic — destroys or retards the growth of microorganisms 

Detergent — improves the cleaning action of water, acts as a wetting agent or 

surfactant to help water penetrate the surface of organic matter, and is 

mildly germicidal 

Disinfectant — inactivates or kills microorganisms, but not necessarily their 

Sanitizer — reduces microbial contamination to a level considered safe 
Sterilizer — destroys all microbes, i 

Resting housing by keeping chickens out for 2 to 4 weeks after cleanup 
helps reduce the microorganism population, since many cannot live long in 
the absence of chickens. 

Drying also reduces the population of microorganisms, but killing a sig- 
nificant number of microbes by drying takes a long lime. 

Sunlight speeds up drying of portable equipment (such as feeders, water- 
ers, cages, and nests) and housing that can be readily opened up to direct rays. 
Sunlight does not penetrate deeply, but will destroy microbes on the surface. 
Sunlight and normal soil activity will effectively disinfect a yard or run from 
which surface organic wastes have been removed. 

Heat produced by composting will destroy most of the bacteria, viruses, 
coccidial oocysts, and worm eggs present in litter. Heap the litter into a pile 
(but not on a wood floor, oryou could start a fire). If the litter is dry, dampen it 
a little to start fermentation. Let the pile heat up to at least 125°F (52"C), leave it 
for 24 hours, then turn it so the outside is on the inside. Let it heat for anodier 
24 hours before spreading the litter back out. Composting litter to destroy its 
microbes is a good idea, whether the litter will be reused for chickens or used to 
fertilize a garden or field. 

Flame is an effective disinfectant, but a hazardous one, especially around 
wood structures. It is best reserved to disinfect concrete pads and to sear away 
feathers stuck to wire cages, but take care: if you hold a torch to galvanized 
wire 1 

22 The Chicken Health Handbook 

Stress Management 

Stress encompasses anything that reduces resistance to disease. Some mi- 
crobes are so strong (or "virulent") that they readily overcome a bird's normal 
resistance. Many microbes, on the other hand, cause no illness or only mild 
illness, unless stress lowers the bird's resistance. 

Some diseases are themselves stress factors — they are not serious, but 
they lower a bird's resistance to a more serious infection. Internal parasites 
(worms) are a prime example of a mild infection diat can open the door to 
something more serious or that can become serious in combination with other 
stress factors. 

No matter how much natural resistance a chicken has, its resistance will 
be reduced to some extent by stress. Stress cannot be avoided. It is normal in 
every chicken's life. Most chickens are able to adapt, even to times of peak 
stress: hatching, reaching maturity, and molting. Additional stresses are 
caused by die environment (such as chilling, heating, and excessive humidity) 
and by routine management procedures (debeaking, vaccinating, and any 
procedure in which birds are handled or herded). 

Stress management involves providing clean, dry litter and range, ad- 
equate protection horn the elements, good ventilation without draftiness, 
contamination-free feed and water, adequate feed and water space, proper 
nutrition, and freedom from crowding. Avoidance of crowding is especially 
important for chicks, since they grow fast and can quickly outgrow their living 
quarters. As birds grow, they develop immunities through gradual exposure to 


Stress reducdon also involves avoiding the indiscriminate or improper use 

when pullets are just starting to lay, when a flock has recently been moved or 
vaccinated, and when the weather is extremely hot or cold. 

Gentle handling as a stress-reduction measure is more important to 
chicken health than fancy housing, according to a study by W. B. Gross at Vir- 
ginia Tech. Gendy treated birds are easier to handle and experience less stress 
during procedures that require handling. Compared to birds that are ignored 
or are treated roughly, birds that are handled gendy grow to a more uniform 
size and are more resistant to infections. 

Preconditioning is another stress-reduction technique. Whenever you 
make a management change, precondition your birds by making the change 
gradually so diat each step is relatively minor. If, for example, you plan to cage 
your pullets for laying, move them at least a week before you expect diem to 
start production. If you plan to move or separate breeders, give them plenty of 

Chicken Health 23 

Showing and Stress 

Showing causes stress by exposing a bird to unfamiliar and confusing sur- 
roundings, strange people, different-tasting water, and any number of new 
and potentially frightening experiences. Excessive showing can be so stressful 
that it affects the fertility and hatchability of eggs. Mens are more easily 
stressed by showing than cocks. 

If you show your chickens, precondition them by coop training them prior 
to the show so they'll get used to being caged alone and handled frequently. At 
show time, bring along your own feed and water — if your chickens don't like 
the feed or water at the show, they won't eat or drink well, dieir stress level will 
go up, and they'll be more susceptible to diseases. Some exhibitors add antibi- 
otics or electrolytes to water during a show, but if a bird doesn't like the taste it 
won't drink, increasing its stress level. 

Stress Behavior 

If you're familiar with the way your chickens normally act, you can readily 
notice changes caused by stress and can take appropriate action. You may be 
able to alleviate the stress behavior through a simple management change. 
Continuing stress that causes long-term behavioral changes seriously reduces 
a chicken's resistance to disease. Sometimes the stress behavior itself is a first 
sign of disease. 

Stress behavior falls into three basic categories: 

• diarrhea 

• labored breathing 

• changes in normal behavior or activity patterns 

Diarrhea becomes evident as a stress sign when you grab a bird suddenly 
and it reacts by pooping on you. Diarrhea can also be a sign that there's some- 
thing wrong with the feed or water or that your birds are suffering from a 
digestive disorder. Labored breathing can be caused by crowding, panic, high 
temperatures, and respiratory distress. Changes in normal behavior or activity 
can be triggered by any number of factors including boredom, fear, crowding, 
constant introduction of new birds, frequent showing, insufficient or unpalat- 
able water, uncomfortable temperatures, and disease. 

The study of animal behavior and its relationship to health is called "vet- 
erinary ethology." For observation purposes, ethologists divide the behavior 
of chickens into eleven distinct areas: 

Reflex behavior involves any automatic reaction, such as flinching or shy- 
ing away from sudden movement. A frightened chicken, for example, might 
shake its head from side to side. A sick chicken reacts more slowly than usual to 
perceived danger. 

Feeding behavior includes both the frequency of visiting feed or water 

troughs and the amount ingested. Undernormal circumstances, a chicken vis- 
its feed and water stations often and eats or drinks a little at a time. Stress 
usually makes a bird eat and drink less, although some diseases increase thirst. 
Anomalous feeding behaviors that call for management action include feather 
picking, cannibalism, drinking excessive amounts of water, eating litter or soil, 
and eating eggs. 

Rest patterns, including sleep, are easily disturbed during times of stress. A 
classic example is restlessness at roosting time, caused by anticipation of being 
bitten by external parasites that feed on birds at night. 

Exploratory behaviorsatisftes the need to investigate new things in the en- 
vironment, including new birds. Excess stress can be induced by the sudden 
introduction of something a bird can't see or doesn't understand (such as the 
loud noise of machinery operating nearby). Excessive stress leads to over- 
reaction, often in the form of flightiness (the "Chicken Little syndrome"). 
Flightiness is relative, however, since some breeds naturally tend to be more 
flighty than others. Anomalous behavior that may be an early sign of disease is 
loss of interest by a bird in its surroundings. 

Body activity relates to motion, including moving from place to place or 
wing flapping for the sheer joy of it. A stressed-out chicken may pace up and 
down, indicating either frustration (as in the case of one cock trying to get away 
from another) or boredom (in the case of a caged chicken). 

Grooming activities include head scratching, preening, mutual grooming, 
and dust bathing. If you're not familiar with dusl-bath behavior, the first time 
you see your chickens laid out in the dirt, you'll surely think they died a sudden 
death. Loss of interest in glooming behavior, so that birds take on a scruffy 
look, is a common early sign of disease. 

Sexual behavior on die part of a cock involves courtship (pecking the 
ground, waltzing, and wing fluttering) and crowing (to establish location and 
warn off competitors — a behavior that's territorial as well as sexual). Sexual 
behavior on the part of a hen largely involves crouching when a cock puts his 
foot on her back in preparation for mating. Hens that are low in the pecking 
order will crouch as the rooster nears and will be mated more often than other 
hens. You can readily identify these subordinate hens by the broken or missing 
feathers on their backs or sometimes by wounds inflicted by the mounting 
cock. Such wounds may be serious enough to require isolation and treatment. 

Parental behavior refers to the relationship between a hen and her chicks, 
since a cock develops no special relationship with his offspring. A hen protects 
her chicks, leads them to feed and water, and communicates with them (and 
they with her) through a series of vocalizations t hat each have a specific mean- 
ing. Anomalous parental behavior includes leaving the nest before the eggs 
hatch (perhaps because the hen was bothered by mites), attacking chicks 
when they hatch, or abandoning chicks. Some breeds, particularly those best 

Ci iic ki;n Health 25 

known for their laying abilities, have been selectively bred not to have the 
brooding instinct. 

Tenitorialism involves aggressive behavior used in an effort to maintain 
personal and territorial space. Crowding increases aggression, which in- 
creases stress. Stress behavior in the form of so-called "displacement" activity 
commonly occurs when one cock of a sparring pair suddenly starts preening 
or pecking the ground. Anomalous territorial behavior includes attacking in- 
truders, other chickens, or humans and refusing (or being unable) to move due 
to fear. 

Social relations in a flock of chickens boil down to the peck order. Birds 
that are low in peck order get chased away from feeders, don't get enough to 
eat, and don't grow as well or lay as many eggs as others. The more birds you 
have, the more importanl it is to have several feeders and waterers, and to 
spread them around. Stress goes up when the peck order is disrupted for any 
reason, such as sickness or the removal or addition of birds. As a result, birds 
eat less, grow slowly or lose weight, and lay fewer eggs. 

Relationship to man starts with imprinting, a phenomenon occurring in 
chicks during their first day of life. By the time a chick is 3 days old, it starts 
experiencing fear, which is why you'll never develop the same friendly rela- 
tionship with mail-order chicks that you can have with chicks hatched in your 
incubator. Whether or not your chickens are imprinted on you, minimize 
stress by talking or singing softly when you work among them, and by moving 
calmly and avoiding abrupt movements. 

The best way to ensure that your chickens are getting a balanced ration is 
to purchase commercially prepared feed designed to suit your flock's stage of 
maturity: chick starter for young and growing birds, layer ration for table-egg 
production, and breeder (or gamebird) ration for hatching-egg production. 
The relationship between health and nutrition is covered in the next chapter. 

HEALTH AND NUTRITION INTERACT in many ways. Disease isn't always 
caused by bacteria, viruses, or other parasites. Disease can also be caused by a 
nutritional deficiency. The nutritional deficiency may, in turn, inhibit the 
body's immune response, opening the door to infection. 

Conversely, an infectious disease may reduce a bird's appetite or inhibit 
absorption of nutrients from its digestive system. The resulting nutritional de- 
ficiencies may either delay recovery or further reduce the bird's resistance, 
increasing its susceptibility to secondary infection. 


Free-ranged flocks are able to forage for natural sources of the nutrients their 
bodies need. Other nutrients are manufactured within their bodies, aided by 
sunlight. Some nutritional deficiencies occur only in chickens confined in- 
doors, away from sunlight. Others occur due to incorrect formulation or 
improper storage of prepared feeds. 

More than thirty-six nutrients have been identified as being essential to 
chickens. Since no single ingredient contains all the necessary nutrients, the 
best ration includes a combination of ingredients that together satisfy a 
chicken's requirements. 

Nutritional problems don't always result from deficiencies, but can be 
caused by excess. Too much of any nutrient, or a lack of balance between 00- 


Health and Nutrition 27 

Free-ranged chickens 
forage for natural 
sources of nutrients. 

trients, can be just as devastating as a deficiency, so don't be too quick to pump 
your birds full of nutritional supplements. 


A chicken's body uses protein to produce antibodies that fight disease. 
During infection, a bird rapidly loses its protein stores, causing its protein re- 
quirement to go up. If the bird cannot obtain additional protein, its resistance 
level drops. 

Feathers are 85 percent protein. Protein requirements tiierefore increase 
during the annual molt, when all of a bird's feathers are replaced with new 
ones. When your flock is about to molt — as indicated by plumage taking on a 
dull look — begin tossing a handful of dry cat food into the yard every other 
day, and continue until the molt is over. Use cat food, rather than dog food, 
because cat food contains animal protein (which is rich in amino acids), while 
most brands of dog food are top-heavy with grains. 

A hard molt — where feathers fall rapidly but grow back slowly — may 
indicate animal protein deficiency. Another indicator is feathers that become 
britde and break easily. If the deficiency is unlikely to be caused by a dietary 
problem, look lor a disease (recent or current) that may be inhibiting protein 

General symptoms of protein deficiency are similar to general symptoms 
of infection: decreased appetite, slow growth in chicks or weight loss in ma- 
ture birds, decreased laying, and smaller egg size. 

Excess protein in a chicken's diet is converted to uric acid and deposited as 
crystals in joints, causing gout. The excess use of meat scraps as a source of 

28 The Ciiickf.n Health Handbook 

protein can also result in an imbalance of phosphorus (described later in this 

Vitamins are divided into two groups: fat soluble and water soluble. The 
fat soluble vitamins (A, D, E, and K) are retained in body fat and used as they 
are needed. The water soluble vitamins (C and the B complex) are not stored 
by the body, which uses only what it immediately needs and expels any excess 
in droppings. Water-soluble vitamins must therefore be replenished more of- 
ten than fat-soluble vitamins. 

Eveiy known vitamin is needed by chickens in some amount. A flock's vi- 
tamin requirements are interrelated widi and must be balanced against other 
nutritional components — protein, minerals, and energy. Of all the nutrients, 
chickens are most likely to be deficient in vitamins A, D, and B2 (riboflavin). 

Caged birds are more prone to vitamin deficiencies than floor-raised 
birds, since the latter pick up some of the vitamins they need from litter. Simi- 
larly, housed chickens are more prone to deficiencies than free-ranged flocks, 
since the latter enjoy a more diverse diet. 

Stress, including disease-induced stress, increases the effects of a vitamin 
deficiency. Heat stress causes birds to eat less and worsens a deficiency. A vita- 
min supplement will give your chickens' immune systems a boost during 
times of stress, such as when their bodies are battling a disease, when the 
weather is unpleasant, during a move, before and after a show, and during 
breeding season. Chicks will get off to a good start if you give them a vitamin 
supplement during their first 3 weeks of life. 

Fat-Soluble Vitamins 

Vitamin A is needed for vision, growth, and bone development. It is called 
the "anti-infection" vitamin because it helps maintain the immune system. It 
also aids disease resistance by playing a role in maintaining the linings of the 
digestive, reproductive, and respiratory tracts. 

Vitamin A deficiency is unlikely to result from improper diet, but may be 
caused by a health condition that interferes with nutrient absorption, such as 
coccidiosis or worm infestation. 

If a chicken misses the mark when pecking, suspect poor eyesight due to 
vitamin A deficiency. An increase in blood spots in eggs may be another sign, 
since the amount of vitamin A needed to minimize blood spots is higher than 
the amount needed to keep a laying hen healthy. 

Vitamin A deficiency can cause nutritional roup which produces respira- 
tory symptoms similar to those of infectious bronchitis or infectious coryza; it 
can also cause the upper digestive tract to develop blisters resembling those of 

Health and Nutrition 29 

fowl pox. The damage caused to linings of the upper digestive and respiratory 
tracts can open the door to bacterial or viral invasion. Deficiency increases the 
severity of respiratory infections such as bronchitis and chronic respiratory 
disease, and increases a chicken's susceptibility to parasites such as coccidia. 

Cod liver oil mixed into mash at the rate of 2 percent is a good source of 
vitamin A. Take care not to go overboard — too much vitamin A is toxic to 

Vitamin D is necessary for the absorption of calcium to make strong 
bones, beaks, claws, and eggshells. A bird's body synthesizes vitamin D from 
sunshine, making deficiency more likely in caged or housed chickens than in 

intended for other livestock, since chickens need vitamin D3 while most other 
stock require vitamin D2. 

A typical sign of vitamin D deficiency is a continuing cycle of normal egg 
production followed by the appearance of thin- and soft-shelled eggs followed 
by a drop in production followed by a return to normal production. A deficient 
hen may have weak legs right before she lays an egg, causing her to squat in a 
penguin-like stance. If the deficiency is not corrected, her beak, claws, and keel 
will become soft and her eggs will be small with reduced hatchability. Defi- 
ciency can be easily corrected by adding cod liver oil to mash at the rate of 2 
percent or by adding vitamin AD&E powder to drinking water three times a 

A chicken's need for vitamin D is intimately tied with its needs for the min- 
erals calcium and phosphorus. A deficiency in any of these three nutrients can 
result in rickets (in young birds) or cage fatigue (in older birds). A deficiency 
may also cause egg eating. 

Excess vitamin D causes kidney damage. One sign of too much vitamin D 
in a hen's diet is calcium "pimples" on eggshells that, when scraped off, leave 
little holes in the shell. 

Vitamin E is necessary for normal reproduction and for resistance to 
Escherichia coli infection (colibacillosis). Wheat germ oil is a good source if 
used fresh — vitamin E in fortified rations degenerates rapidly, especially 
when temperature and humidity are high. Deficiency is most likely to occur in 
confined young birds fed a diet that's high in soy bean oil or cod liver oil and in 
birds fed rations containing rancid fats. Deficiency in chicks can result in 
encephalomalacia, exudative diathesis, or white muscle disease. Deficiency in 
cocks can cause loss of fertility. 

Vitamin K\s necessary for normal blood clotting. Signs of deficiency are 
profuse bleeding from slight wounds and internal bleeding (under the skin or 
into the body cavity). Vitamin K may trigger infectious anemia, especially in 
chicks treated for extended periods With the coccidiostat sulfaquinoxaline. Al- 

30 The Chicken Health Handbook 

Water-Soluble Vitamins 

Vitamin B is actually a whole group of unrelated substances whose names 
change so olien it's hard to keep up. Vitamin B deficiency was not an issue in 
the days when chickens roamed pastures, freely picking in cow patties and 
horse apples. Health problems occurred when breeders started to specialize 
and began penning their chickens. In those early days, poultry keepers kept 
dieir flocks healthy by tossing them fresh horse or cow manure, but no one 
knew why it worked until 1948, when researchers discovered that manure con- 
tains vitamin B12. This B vitamin is i 

almost exclusively in animal products. 

Today, deficiency is not a problem where poultry keepers have returned to 
the practice of letting chickens run with other livestock. Chickens raised on 

Vitamin Benefits and Sources 


B complex 

thiamin (Bl) 
riboflavin (B2) 

nicotinic acid 

pantothenic acid 
biotin (H) 


benzoic acid 

folic acid (folacin) 


cod liver oil 


vision, growth, bone develop- 
ment, resistance to diseases & 

leafy greens, grass, milk, 
many sources 

many sources 

brewer's yeast, leafy greens, 
many sources 
yeast, many sources 

many sources 
green leaves 
meat protein 

_ growth & 

cod liver oil 
AD&E powder 

wheat genn oil 
AD&E powder 

alfalfa leaves 

strong bones, beaks, claws. & 
eggshells; hatchabiliry 

fertility, resistance to 

normal blood clotting 

Health and Nutrition 31 

built-up floor litter get enough vitamin B12 by picking in the litter. Deficiency 
can occur in housed flocks, especially those fed soymeal as the sole or main 
source of protein. 

Curled-toe paralysis in chicks is a sign of riboflavin (vitamin B2) defi- 
ciency, occurring when penned breeder hens are fed unsupplemented lay 
radon. Greens, including young grass, are good sources of riboflavin. Milk, 
whey, and other dairy products are also good sources, but too much can cause 

All the B vitamins, along with other vitamins, are added to commercial ra- 
tions and are otherwise so readily available in a wide variety of feedstuff's that, 
in a properly managed flock, deficiency is unlikely. 

Vitamin Chelps prevent diseases by reducing the harmful effects of stress. 
Chickens make dieir own vitamin C and do not need a supplement except 
when the absorption of vitamin C and other nutrients is inhibited by stress, 
such as might be induced by high environmental temperatures. 


While vitamins have their origins in organic plant or animal matter, min- 
erals are inorganic elements. They give bones rigidity and strength, and diey 
interact with other nutrients to keep the body healthy. Just as caged birds are 
more prone to vitamin deficiencies than floor-raised birds, they're also more 
prone to mineral deficiencies. But, unlike vitamins, minerals do not go stale. 
Most commercial feeds contain adequate amounts, with the possible excep- 
tion of calcium. 

Calcium and phosphorus are needed by chicks for bone formation and by 
hens for eggshell formation. Calcium and phosphorus are interrelated, and 
both require the presence of vitamin D to be metabolized. A deficiency in vita- 
min D can cause a deficiency of calcium and/or phosphorus. 

Regardless of the cause, a deficiency of calcium and phosphorus increases 
a chicken's susceptibility to parasitic infection. Beetles and other hard-shelled 
bugs contain lots of calcium and phosphorus; ironically, they may also be a 
source of parasitic infection. A good supplemental source of calcium is ground 
oyster shells or limestone (but not "dolomitic" limestone, which can inhibit 
egg production). 

Older hens need more calcium than younger hens, and all hens need more 
calcium in warm weather. Rough eggshells are a sign that a hen is getting too 
much calcium. 

Magnesium is needed for bone formation, eggshell formation, and the 
metabolism of carbohydrates. A chicken's diet is more likely to have too much 
magnesium than too little, leading to diarrhea and smaller eggs witii thin shells. 

32 The Chicken Health Handbook 

causing chicks to grow slowly and hens to abruptly lay fewer, smaller-sized 
eggs, lose weight, and become cannibalistic. But chickens are more likely to get 
too much salt than too little. The result is increased thirst, inability to stand, 
weak muscles, convulsions, and death. A lethal dose of salt is 0.06 ounce per 
pound (4g/kg) of body weight. 

Chicks are more susceptible to salt poisoning than adults. Salt poisoning 
can occur when a flock's sole source of drinking water is saline water, although 
chickens can tolerate salt in water up to 0.25 percent. Poisoning can also occur 
when chickens pick in rock salt used for de-icing sidewalks and driveways. 

Salt poisoning can be caused by a normal amount of salt in rations during 
summer, if chickens run out of water, and during winter, if drinking water 
freezes. Obviously, the way to avoid salt poisoning is to be sure your chickens 
have fresh, clean water at all times. 

Potassium deficiency can occur during times of heat or other stress, result- 
ing in decreased egg production, thin shells, and general weakness. 

Manganese is needed for normal bones, for good eggshell quality, and to 
prevent slipped tendon. Coccidiosis interferes with its metabolism. 

Copperdeficiency can cause a loss of feather color in New Hampshires and 
Rhode Island Reds. As with manganese, t 
by coccidiosis. 

Selenium deficiency is associated with white muscle disease; an excess of 
selenium increases susceptibility to salmonellosis. Corn and other grains may 
be low in selenium if they are grown east of the Mississippi River and in the 
Pacific Northwest, where the soil is selenium deficient. Grains may be espe- 
cially high in selenium if they are grown in the Great Plains or parts of Canada 
where soils contain an excess of selenium. 


A chicken's protein requirement goes up during the annual molt, its vita- 
min and mineral needs remain fairly constant year around, and its energy 
requirements fluctuate with outside temperature. Where die temperature 
range is extreme, energy must be adjusted seasonally — upward during cold 
months, downward during warm months. Energy can be lowered by adding 
wheat bran (but too much affects laying). Energy can be increased by increas- 
ing protein or carbohydrates. 

Although protein contains a certain amount of energy, the cheapest form 
of energy is carbohydrates found in cereal grains. Grains are also the most ca- 
loric form of energy, so diey must be used judiciously. Since a chicken eats to 
satisfy its energy needs, if its ration is too high in carbohydrates, the bird gets 
fat; if too low. the bird becomes underweight. In bodi cases, the bird is more 
susceptible to disease. 

Hkalth and Nutrition 33 

Chart 2-2 

Nutritional Diseases and Disorders 

Disease caused by: 

Deficiency of: 

excess oj. 

Cage fatigue 


Curled-toe paralysis 

(vitamin B2) 

Egg binding 

calci u m / phospho rus 


vitamin E 

Exudative diathesis 

vitamin E 

Fatty liver syndrome 





IlllcCllUUo eUldma 

V I Ldl 1 11 1 1 1*. 

Prolapsed oviduct 

calcium / phosphorus 


vitamin D 

Roup (nutritional) 

vitamin A 

Slipped tendon 




White muscle disease 

vitamin D 
vitamin E/selenium 

Nutritional Diseases 

Nutritional research has traditionally focused on broiler chicks and laying 
hens. More is therefore known about the requirements for rapid early growth 
in heavy breeds and about the maintenance needs of light laying breeds than 
about the requirements of breeder flocks, especially in the heavy breeds. Com- 
mercial feeds designed for mature birds are formulated for maintenance, 
ensuring that hens lay well but not necessarily providing sufficient nutrition 
for die eggs to develop into strong viable chicks. (See chapter 13 for more about 
the influence of nutrition on the hatehability of eggs and viability of chicks.) 

Chickens, like humans, depend for good health on the existence of benefi- 
cial bacteria and other microorganisms living in their digestive tracts. A bird's 
nutritional requirements go up when the delicate balance of these microflora 
is upset by illness, drugs, stress, or an abrupt change in feed. 

A bird's nutritional requirements can also be increased by any condition 
diat causes nutrients to be destroyed before they can be absorbed or diat in- 
hibits the chicken's ability to absorb them. Interference with the absorption of 
nutrients, called "malabsorption," can be caused by parasite loads including 
worms or coccidia, infection, drug use, and environmental stress due to low 
humidity or temperature extremes. Any of these conditions can make even the 
most perfectly formulated rations insufficient to prevent a deficiency. 

34 The Chicken Health Handbook 

Deficiency Symptoms 

A nutritional deficiency may be: 

• borderline — resulting in slow growth, poor or rough feathering, lack 
of energy, lack of appetite, a slight drop in egg production, and slightly 
reduced hatchability; 

• serious — birds become crippled, hens stop laying; 

• extreme — ending in deaUi. 

Nutritional diseases tend to be quite similar to one another, making it hard 
to tell specifically which nutrient is lacking. In addition, deficiencies are rarely 
simple (having a single cause) but are more likely to be multiple (caused by the 
lack of more than one nutrient). Symptoms of a simple deficiency are deter- 
mined by deliberately putting chickens on a deficient diet and observing the 
results. In a real-life multiple deficiency, symptoms combine to complicate the 

Chart 2-: 

Nutritional Symptoms 

Body Part Disease/Condition 









excessive bleeding 

greenish yellow 

loose & ninny 

blood spots 

pale yolk 
calcium pimples 
low fertility 
low hatchability* 

low production 

vitamin D 
vitamin K 
vitamin D 
vitamin D 
vitamin E 
vitamin D 

vitamin A 

vitamin E 



vitamin A 





vitamin A 
vitamin D 

vitamin A 

Health and Nutrition 35 

Body Part 



Ebbs (cont.) 

on 1 * 

no production 


soft shell 

calcium/vitamin D 

thin shell 


vitamin D 

no shell 

vitamin D 

eating of 


vitamin D 



vitamin A 

nfin - vision 

vila in in A 

V) till! III! i \ 


vitamin A 

V 1 Ifll 1 111 I / \ 


black in ermine nattern 

vitamin D 

» UMM III 1 I—' 





hard moll 

nrol pin 


n rotein 

pale, in black & red breeds 



vitamin A 



vitamin D 


stiff Wrilk 

'III VtUJ1\ 


nptiPiiin sciiifil 

J 1 '. 1 1 ... 1 ! M 1 " 1 1 ! . 1 1 

vitamin P) 

VII (11 1 11 1 1 IS 

weak or bowed 

vitamin D 


whitish sores 

vitamin A 


swollen joints 

vitamin D 

weak musrlps 

vitamin F 

V 1 1(11 1 1 1 1 1 1 —i 


ppnpral svmotnm^ 

vitamin A 

VII UI 1 llll t X 


collapsed (adult) 

vitamin D 

hpaHpfl frhirk^ 

vilamin Fl 

> 1 1(11 1111 I U 



' VIA llv V* 




vitamin A 

V A LU-1 lllll J 1 


vitamin F 

V 11(1111111 I_- 


calcium & phosphorus 


slipped tendon 




vitamin A 


slow growth 


vitamin A 

vitamin D 

weight loss 









*See "Nutrition-Related Hatching Problems," p. 217. 

36 Ti m Ci iicken Health Handbook 

Certain feedstuffs diemselves affect digestion and nutrient absorption. The 
growth rate of chicks, for example, is retarded by uncooked soybeans and 
soymeal. Deficiencies sometimes occur when commercial feeds are manufac- 
tured under new technologies. When processors switched from the expeller 
method to the solvent method of extracting soybean meal, feeds were deficient 
in folic acid and had to be reformulated to include an increased amount of that 
B vitamin. Even feedstuffs that are high in nutrients may contain them in 
"bound" form, meaning the nutrients are unavailable to or poorly utilized by 

If you stockpile feed or continuously buy from the same stockpiled source, 
diagnosis of a nutritional deficiency may involve analyzing your feed. For most 
small flocks, though, feed is bought in small batches, and one batch is not likely 
to be around long enough to cause a serious deficiency, let alone be analyzed 
for its nutritional content. 

A good rule of thumb is to buy only as much feed as you can use \ 
weeks of manufacture. Store the feed in such a way that it won't go ranc 
moldy, or stale. Mold and other spoilage organisms destroy nutrients, and 
even the best commercial rations lose nutritional value during prolonged stor- 
age at a warehouse or on your back porch. Despite the inclusion of 
antioxidants to retard deterioration, nutrients are destroyed over time by beat, 
sunlight, and oxygen. 

Feeding Schedule 

Flock Type 


Roasters and Capons 
Layers and Breeders 

1 day-5 weeks 
5-7 weeks 
or 1 day-7 weeks 

starter/ grower 

7 weeks-slaughter finisher + corn 

1 day-6 weeks 
6-13 weeks 
13-20 weeks 
or 1 day-20 weeks 
20 weeks 


pullet developer 
starter/ grower 
lay ration + oyster shell 
or limestone grit 

*In many areas, the only feeds readily available for small flocks are starter/grower and lay 
ration. Gradually make any feed change by adding progressively more of the new ration until 
the changeover is complete. and Nutrition 37 

Nutritional content holds up best in feed stored in a cool, dry, place, away 
from direct sunlight. Once you open a bag, transfer its contents to a sealed 
container such as a clean plastic garbage can with a tight-fitting lid; don't store 
feeds in metal cans, which sweat in warm weather, causing the feed to go 
moldy. Never feed chickens moldy rations, whether the mold developed in a 
storage container or in a sack that got wet. 

Avoid cheap feeds that don't contain animal protein or high-fiber ingredi- 
ents such as alfalfa or wheat products. Such feeds start out missing nutrients 
and go downhill from there. Also avoid the temptation to save money by feed- 
ingyour flock copious amounts of scratch grains or stale bakery products, both 
of which will upset the nutritional balance of even the best feeding program. 
Corn and other treats should never make up more than 5 percent of a flock's 
total diet. 



Space per Bird 

2.5 cm 
5.0 cm 
7.5 cm 

Feeder design can affect health by 
allowing droppings to accumulate in 
the feed. Droppings can be excluded 
jders from the rafters or 
by fitting them i 
rotate and dump 
roost on diem. 

Feeder design can also affect 
health by allowing feed to be scattered 
on the ground, where it not only at- 
tracts rodents but combines with 
manure and moisture to provide a 
good environment for disease-caus- 
ing organisms. Billing out (the bad habit chickens have of using their beaks to 
toss feed out of a trough) can be prevented by using a feeder with an inwardly 
rolled lip and by positioning the feeder so the hopper is approximately the 
height of the birds' backs. Here, again, a hanging feeder is ideal because its 
height can easily be adjusted as birds grow. 


0- 6 weeks 1 .0" 

7- 18 weeks 2.0" 
1 9 weeks and up 3.0" 


1 day-1 week 

1- 4 weeks 
4-8 weeks 

8- 20 weeks 
21 weeks and up 


2.5 cm 
5.0 cm 
5.0 cm 
4.0" 10.0 cm 
5.0" 12.5 cm 

Feed Amount 

How much chickens eat varies with the ration's palatability, texture, en- 
ergy, and protein content, as well as with the chickens' breed and strain, 
degree of activity, and condition of health. How much a chicken eats also var- 
ies with environmental temperature. Chickens subjected to cold winter 
temperatures need more feed than chickens raised in a wann climate or in a 

38 The Chicken Health Handbook 

controlled environment. Hot weather causes a chicken to eat less; the ration's 
nutritional value must therefore be increased to meet the bird's needs. 

Depending on their breed and purpose, chickens may be either fed free 
choice (given a constantly ready suppy) or placed on a restricted feeding 
schedule. Broilers and roasters should be fed free choice, since the idea is to get 
them to butchering age as quickly as possible. Pullets of the lightweight laying 
breeds may also be fed free choice, since they have been bred for efficient feed 

Older lightweight hens, as well as breeders in die dual-purpose or meat 
categories, should be kept on a restricted diet. Restricting the feed intake of 
pullets past the age of 4 weeks slows their growth and delays the onset of lay- 
ing, causing them to do better when they become layers and/or breeders. 
Restricting the intake of mature breeders keeps them from getting unhealthily 
fat and developing fatty liver syndrome. 

Restricted Feeding Schedule for Pullets 


Body Weight* 

Feed per 







Laying Breeds: 














































Meat Breeds: 














































*To age 4 weeks, each layer pullet averages 1 .47 pounds (672 grams) of feed, each broiler 
pullet averages 1.09 pounds (954 grams). 

**Average expected body weight under restricted feeding program. 

Health and Nutrition 39 

Rations-Related Problems 

Starvation occurs when newly hatched chicks do not leam to eat quickly 
enough, causing them to lose energy rapidly until they can no longer actively 
seek food. In older birds, starvation occurs when rations are too high in fiber 
(common in cheap feeds). Starvation may also be related to climate: during 
cold weather, chickens may not get enough to eat to keep warm; during ex- 
tremely dry weather, vegetation may be scarce for free-ranged chickens. 

Obesity is most likely to occur in chickens kept as pets and in caged birds 
that are inactive and therefore eat more energy-rich feed than they need. Some 
breeds, especially New Hampshires and other dual-purpose breeds, have a 
natural tendency to put on fat. Fat hens do not lay well and are prone to heat 
stroke, reproductive problems, and fatty liver syndrome. 

Xanthomatosis, a condition in which thick yellow or orange patches ap- 
pear on the skin, is apparently caused by toxic fats in rations. 


A chicken's body is 50 percent water and an egg is 65 percent water, making 
water the most important nutrient in a chicken's diet. Water serves many func- 

Chakt 2-7 

Diseases Affecting 
Water Consumption 

Increase Decrease 
Consumption Consumption 

Blackhead Infectious coryza 

Cholera Omphalitis 



Infectious bursal 


Newcasde disease 



Chart 2-8 

Diseases Related to 
Drinking Water 



Algae poisoning 

algae toxins in 

surface water 


stress triggered by 

lack of water 


rotting organic 

matter in water 


insufficient drinking 


Salt poisoning 

insufficient or saline 

drinking water 


water contaminated 

with fungus 

Numerous bacteria, proiozoa, and viruses 
are spread by means of drinking water 
contaminated with droppings or mucus from 
infected birds. 

40 The Chicken Health Handbook 

tions; among them is to transport other 
nutrients throughout the body and to 
keep the body cool through evapora- 

An old saying points out the perver- 
sity of chickens: "A flock's water supply 
is no better than the poorest drinking 
water available." You can bring your 
flock the purest, freshest water, yet 
your birds will persist in drinking from 
filthy puddles. Good yard drainage pre- 
vents stagnant puddles in which 
disease-causing microbes and para- 
site-carrying insects thrive. If your soil is neither sandy nor gravelly, enhance 
drainage by locating your coop on a slight slope. Many microbes and parasites 
can't survive long in the absence of moisture. 

Provide your flock with water from a clean, reliable source. Avoid surface 
tanks, ponds, or streams, all of which are easily contaminated. Chickens prefer 
drinking water with a temperature of about 55°F (13°C), and will drink less if 
water is much above or below that. 

The average chicken drinks between 1 and 2 cups (237 to 474 ml) of water 
per day, depending on numerous factors including its size, the environmental 
temperature, water palatability, feed intake, feed composition, condition of 
health, and whether or not die bird is laying. 

The average layer drinks twice as much as the average non-layer. Some 
disease conditions cause chickens to drink more, as do rations that are high in 
protein or salt. Chickens drink less if the water contains medication or an ex- 
cessive amount of dissolved minerals that die birds find unpalatable. Chickens 
dial don't drink enough because water is unpalatable, dirty, or warm (or there 
simply isn't enough) can die from kidney failure. 

Under normal conditions, a chicken will drink approximately twice as 
much as it eats, by weigh t. A layer, for example, may eat »/ 2 pound (224 g) of feed 
and drink 2 cups (474 ml) of water per day. As the temperature goes up, the 
ratio of water to feed also goes up, as high temperatures cause a chicken to eal 
less and drink more. 


A chicken can survive longer widiout feed dian without water. Chickens 
drink only a little at a time, so they must drink often. Insufficient water slows 
growth in chicks and reduces egg production in hens. 

Chart 2-9 

Environmental Temperature 
and Water Consumption 


of Water to 
Temperature One Pan Feed 



1.8 parts 













HEALTH and Nutri tion 41 

Signs of Water Deprivation 

maybe available to chicks, but perhaps 
they are too small to reach it. Chickens 
of any age will be deprived of water if 
the water quality is poor or they simply 
don't like the taste of it. Diarrhea 
causes dehydration by passing water 
through the body too quickly to be ab- 
sorbed. Hens may have plenty of water 
in winter, but if the water freezes, egg 
production will drop. In warm 
weather, water deprivation occurs 

when a flocks water needs go up but the supply remains the same. 

If a laying hen goes without water for as little as 24 hours, she may take as 

Body Part Change 

Comb and wattles 


and bluish 

Tendons on backs 

stand out 




off color 

long as 24 days to recover. I 
into a molt, followed by a li 
never recover. 

water for 36 hours, she may go 
iod of poor laying from which she may 



Waterer Space 

Trough/Bird Birds/Fount Caged Birds/Cup 



0-6 weeks 

1.0" 2.5 cm 100 



7-18 weeks 

1.0" 2.5 cm 50 



19 weeks and up 

2.0" 5.0 cm 30 



Founts or Cups/ 1 00 Birds 


1 day-1 week 

1.0" 2.5 cm 1 

1-8 weeks 

1.0" 2.5 cm 2 

8 weeks and up 

1.0" 2.5 cm 2 


1.0" 2.5 cm 2* 

Minimum Water Needs 


Water Per Dozen Birds 

1 day-1 week 

1 quart 1 liter 

1-4 weeks 

2 quarts 2 liters 

4-12 weeks 

1 gallon 4 liters 

12 weeks and up 

1.5 gallons 6 liters 

*Double in hot weather 

42 The Chicken Health Handbook 


A good waterer is designed so chickens can't step in the water or roost over 
it, and it holds enough to last until it can conveniently be refilled. Automatic 
watering is, of course, ideal, provided you check it daily to make sure die sys- 
tem is functioning properly. Once a week, add 1 tablespoon of sodium 
bicarbonate (baking soda) per gallon to the automatic watering tank to keep 
slime from forming in the pipes, valves, and drinkers. Diseases can be spread 
through drinking water, so clean and disinfect all waterers regularly. 

In winter, coils or a heating pan will keep water from freezing. In summer, 
place waterers in a shady place where the water won't be wanned by the sun. A 
gravel or sand bed beneath the waterer, topped with droppings boards, will 
keep chickens from drinking spills and picking in moist, filthy soil diat invari- 
ably surrounds a waterer. 

Anatomy of a Chicken 

ferent ways. When a bird gets sick, knowing what part of its body is affected 
may help you determine what disease the bird has. 

If your flock keeps getting diseases that always affect the same body sys- 
tem, some management change may be in order. Frequent bouts with 
digestive disorders, for example, may indicate a need for improved sanitation, 
while repeated respiratory problems may signal a need for improved ventilation. 

Vital Statistics 

Maximum Life Span: 30-35 years 
Maximum Productive Life: 12-15 years 
Body Temperature 

adult 103°F(39.5"C) 
chick 106.7°F(41.5°C) 

Respiratory Rate 

Heart Rate* 

cock 12-20breaths per minute 
hen 20-36 breaths per minute 

adult 250-350 beats per minute 
chick 350-450 beats per minute 

*Heart rate varies with breed and sex; a mature New Hampshire cock has a heart 
rate oF250 beats per minute, a mature Leghorn hen 350 beats per minute. 


44 The Chicken Health Handbook 

Immune System 

A chicken's first defense against disease is its skin, the largest organ and the 
main one by which a bird comes into contact with its environment. The major- 
ity of disease-causing organisms can enter a chicken's body only through the 
skin protecting the outside of its body or the mucous membranes lining the 
openings on the inside of its body. 

On the skin live certain microbes that, through competition, keep other 
microorganisms away. If the skin is broken, even these "good" microbes may 
get into the body and cause disease. Microbes have an easier time getting 
through mucous membranes than through the skin. They are kept out by mov- 
ing fluids (mucus and tears) and by enzymes that destroy invaders. 

If a microorganism manages to breakthrough the defenses of the skin or 
mucous membranes, the bird's lymphatic system takes up die battle. All body 
tissues are lubricated by watery fluid, called "lymph," that's derived from the 
bloodstream and that accumulates in the spaces between tissue cells. The 
lymphatic system drains lymph from all over the body and returns it to- the 

out microbes and oUier foreign bodies. 

Lymph contains specialized white blood cells of several kinds, technically 
called "lymphocytes" but popularly known by such names as "engulfing" 

Where antibodies are produced 


Anatomy or a Chicken 45 

cells and "killer" cells. Lymphocytes 
neutralize or destroy invading mi- 
crobes, which they recognize as 
antigens. An antigen is, quite sim- 
ply, a protein diat differs from any 
natural protein in the body. 

When lymphocytes detect an 
antigen, they respond by producing 
substances to fight the invader. 
These substances are called "anti- 
bodies" or "immunoglobulins." No 
one knows exactly how antibodies 
are produced. What is known is that antibodies attach themselves to antigens, 
maidng it easier for engulfing cells, killer cells, and other lymphocytes to de- 
stroy the antigens. 

Antibodies are also produced by the spleen (the additional function of 
which is to remove and destroy worn-out blood cells). Many diseases affect the 
spleen, causing it to swell (paratyphoid), turn mushy (histoplasmosis), or atro- 
phy (infectious anemia). The spleen is not a vital organ, however, and if it 
ceases to function, other parts of the body take over its job. 

Immunity is controlled and antibody production is activated in chicks by a 
rose-shaped organ behind the cloaca, called the "cloaca! bursa" (or "bursa of 
Fabricius"). Some viral diseases damage the cloacal bursa, permanently com- 
promising the bird's immune system. Infectious bursal disease, die most 
common cause of immunosuppression, is a fairly common infection of chicks 
3 to 6 weeks old that attacks lymph tissue and destroys the cloacal bursa. 
Marek's disease, a common tumor disease of birds 3 to 6 months old, may also 
damage the cloacal bursa. 

Location of cloacal bursa, organ responsible for antibody production 

Diseases Involving the 
Cloacal Bursa 

Disease Effect 

Infectious anemia atrophy 

Infectious bursal disease atrophy 

Lymphoid leucosis tumor 

Marek's disease tumor 

Runting syndrome atrophy 


46 The Cmqim Health Handbook 

Digestive System 

A chicken has no teeth. Saliva starts breaking down feed as soon as it enters the 
bird's mouth. Its tongue pushes the feed toward the back of its mouth. The 
feed then slides down the esophagus, a tube leading to Ore crop where the feed 
is temporarily stored. You can sometimes see a full crop bulging at the base of 
a bird's neck. 

Occasionally the crop becomes impacted (see "Crop Impaction," page 
264). Crop impaction may occur when feed is withheld preparatory to worm- 
ing, causing chickens to eat too much at once afterward. Crops may also get 
packed when birds are free ranged where little is available to eat but tough, 
fibrous vegetation. Even if the bird continues to eat, nutrition cannot get 
through. The swollen crop may cut off the windpipe, suffocating die bird. Crop 










Anatomy of a Chicken 47 

From the crop, feed is moved to the proventriculus or true stomach, where 
enzymes break it down further. It is then passed along to the gizzard, or me- 
chanical stomach, an organ with strong muscles, a tough lining, and a 
collection of small stones or grit for grinding up grains. 

A chicken fed only commercially prepared mash or pellets does not need 
grit. Its digestive efficiency will be impaired, however, if it eats grains without 
having access to grit for its gizzard. If a bird eats a small, sharp object such as a 
tack or staple, the object is likely to lodge in its gizzard and, due to the strong 
grinding motion of the gizzard muscles, may eventually pierce the gizzard 
wall. As a result, the bird will grow thin and eventually die — a good reason to 
keep the yard free of nails, glass shards, bits of wire, and the like. 

From the gizzard, feed passes into the small intestine for absorption. The 
upper portion of the small intestine, called the "duodenum," forms a loop. 
Enclosed by the duodenal loop is the pancreas, which secretes enzymes to aid 
digestion, bicarbonate to neutralize acids, and hormones to regulate blood 

Between die duodenal loop and the lower small intestine is connected the 
liver, an organ t hat secretes green bile (or gall) to aid in the absorption of fats in 
the intestine. Attached to the liver is a transparent pouch, the gall bladder, 
where bile is stored until it is needed. 

Branching off between the small and large intestine are two blind 
pouches, called the "ceca" (one is a "cecum"), that have no known function. 
The ceca empty their contents two or th ree times a day, producing pasty drop- 
pings that often smell worse than regular droppings. 

The last portion of the intestine, the large intestine or "rectum," is rela- 
tively short. It absorbs water from feedstuff's as they pass through. 

Both the small and large intestine are normally populated by beneficial 
bacteria, referred to as "microflora" (micro meaning very small and flora 
meaning plants). Microflora aid digestion and enhance immunity by guarding 
their territory against invading microbes. An intestinal disease occurs when 
the balance of microflora is upset or the normal microflora are overrun by too 
many foreign organisms (usually eaten in contaminated feed or water). The 
result is enteritis or inflammation of the intestines; symptoms include diar- 
rhea, increased thirst, dehydration, loss of appedte, weakness, and weight loss 
or slow growth. 

Enteric diseases tend to be complex. Combinations of and interactions 
between various organisms — worms, bacteria, protozoa, viruses, and natural 
microflora — determine the severity of the disease. Successfully treating 
enteritis requires knowing what organism, or combination of organisms, is 
causing the illness. 

The large intestine ends at the cloaca, where the digestive, reproductive, 
and excretoiy tracts meet. The cloaca has three chambers: 

48 The Chicken Health Handbook 

• the fecal chamber, ai the end of the rectum 

• the urogenital chamber, where the excretory and reproductive systems 
come together 

• the vestibule, into which the cloacal bursa empties 

In the fecal chamber, a final bit of moisture is absorbed from feedstuffs 
leaving the body, which are then expelled through the vent in the form of drop- 
pings. In a healthy chicken, feed passes through the entire digestive system in 3 
to 4 hours. 

Excretory System 

The excretory system consists basically of the kidneys (lying along the 
chicken's back) connected to the cloaca's urogenital chamber by means of 
tubes called "ureters." The kidneys are responsible for filtering and removing 
wastes from the blood. In humans, these waste products are expelled in urine. 
A healthy chicken does not excrete urine, but expels blood-wastes in the form 
of semi-solid uric acid, called "urine salts" or "urates," that appear as white, 
pasty caps on droppings. 

Urates may be improperly metabolized due to water deprivation, excess 
dietary protein or calcium, or certain diseases. Droppings may then contain 
more than the usual amount of urates (as occurs in spirochetosis), or urates 
may accumulate as pasty deposits in the joints (articular gout) or collect as 
crystals that block the ureters (as in the case of infectious bronchitis). 

The function of the respiratory system is to circulate oxygen throughout die 
body and to aid in temperature regulation. Parts of the respiratory system in- 
clude the nose, diroat, trachea or windpipe, lungs, air sacs, and certain bones. 
Chickens, like other birds, are peculiar in having an extensive system of air 

die body. The system of air sacs extends around the internal organs and into 

Air Sacs 

Number Name 


2 abdominal 

1 cervical 

2 interclavicular 

2 thoracic, anterior 

2 thoracic, posterior 

surrounding intestine 
neck, above esophagus 
beneath lung 
behind lung 

Anatomy of a Chicken 49 

Respiratory System 

some bones, called "pneumatic" bones, that are hollow. While the lungs are 
rigid, air sacs are flexible. All but one come in pairs. The largest pair is in the 
abdomen, surrounding the intestine. 

Respiratory Disease 

Respiratory disease has always been a problem in poultry. At one time, all 
respiratory diseases were lumped together as "colds" or "roup." During the 
middle part of the 20th century, they were recognized as a group of separate, 
sometimes unrelated, infections with common characteristics similar to a hu- 
man cold: labored breathing, coughing, sneezing, sniffling, gasping, runny 
eyes and nose. 

In these modern times, respiratory diseases are classified according to 
their cause, whether nutritional, parasitic, bacterial, fungal, viral, or environ- 
mental. Most serious respiratory diseases are caused by viruses, for which 
there is no cure and which are easily spread in moisture expelled by a sick bird 
that coughs, sneezes, or simply breathes. Respiratory distress can also occur as 
a reaction to vaccination, especially against Newcastle disease or infectious 

1, so that a i 

of one disease may continue to have symptoms produced by a second disease. 
The best defense against respiratory illness is to develop your flock's genetic 
resistance. The best management practices are to provide good ventilation 
and avoid introducing carriers into your flock. 

Skeletal System 

The skeletal system of a chicken has diree functions: 

• to support the bird 

• to transport calcium 

• to aid respiration 

Respiration is aided by a system of hollow pneumatic bones. Calcium 
transport is aided by a system of so-called "medullary" bones, from which a 
hen gets 47 percent of the calcium used in eggshell formation. 

Skeletal problems can be caused by insufficient calcium, either because 
the diet is deficient or because a disease or other condition keeps calcium from 
being properly metabolized. Common problems include crooked or humped 
back, crooked keel, and wry tail (that flops to one side). 

By far the most common problem is weak legs, which may be related to 
genetics, nutrition, infection, or some combination thereof. In hens, the prob- 
lem is usually the result of mineral 
imbalance. Leg weakness is more 
likely to occur in heavy breeds than in 
light breeds. Guard against it by keep- 
ing young birds off slippery surfaces, 
by feeding a balanced diet, and by not 
breeding lame or deformed birds. Be 
aware that lameness is not always a 
skeletal disorder, but may result from 
nerve or muscle damage. 

Another common skeletal problem 
is inflammation of the joints and syn- 
ovial membranes — thin membranes 
lining joint cavities and tendon 
sheaths. The synovial membranes se- 
crete synovia, a fluid resembling thin 
egg white that lubricates joints. 
Inflammation of the synovial mem- 
branes, called "synovitis," causes 
excess synovia to be secreted, making 
the joint swell and become warm and 

Anatomy or- a Chicken 51 

painful. The most likely joini affected is the hock. Non-infectious synovitis 
may be caused by injury or nutritional problems. Infectious synovitis may be 
caused by bacteria, staphylococci, or viruses, 

Near the joints, at places where a tendon or muscle crosses a bone or 
muscle, are small, fluid-filled sacs, called "bursa," that cushion pressure 
points. Inflammation of the bursa (bursitis) can be caused by pressure, fric- 
tion, or injury to the membrane surrounding the joint. If the bird is not 
rei injured or does not become infected, after a time the excess fluid is re- 
absorbed by the bloodstream. The most common form of bursitis is keel 
bursitis, popularly known as "breas: blister." Breast blister is caused by pres- 
sure against dne keel, usually in a bird with weak legs (so it cannot keep its 
weight off the keel while resting) and/or poor feathering (that offers little pro- 
tection to the keel). 

Reproductive System 

A cock's reproductive system consists of two sperm-producing testes and the 
accompanying equipment necessary to get the sperm into a hen. A hen's re- 
productive system consists of one ovary and a passageway or oviduct that's 
slightly more than 2-feet long. 

A female chick embryo actually starts out with two ovaries, but the right 
one atrophies. Only the left one continues to develop and become functional. 
For some unknown reason, occasionally the right oviduct develops partially 
and becomes cystic, eventually growing so large it presses against other inter- 
nal organs and causes death. 

The functioning left ovary consists of a clump of undeveloped yolks or ova 
(one is an "ovum") located just beneath the hen's backbone, approximately 
halfway between the neck and tail. As each ovum develops and matures, it is 
released into Une oviduct, usually about an hour after dne previous egg was laid. 
Double-yolked eggs, laid most often by pullets and by heavy-breed hens, occur 
when two yolks are released within 3 hours of each other. 

During a yolk's jounney dnrough the oviduct, it is fertilized (if sperm are 
present), encased in albumen or egg white, wrapped in a membrane, and 
sealed in a shell. The whole process takes about 25 hours, causing a hen to lay 
her egg a little later each day. Since a hen rarely lays in the evening, as dne cycle 
progresses she'll eventually skip a day and start a new cycle the following 
morning. A group of eggs laid within one cycle is called a "clutch." A hen with 
a longer cycle (say, 28 hours) lays fewer eggs per clutch than a hen with a 
shorter cycle. 

Any interruption in normal cycling can result in abnormal shell patterns. 
Abnormal patterns also occur when yolks are released less than 25 hours apart, 
causing two eggs to move through the oviduct close to each other. The second 

52 Tut; Chicken Handbook 

Reproductive System of a lien 

egg will have a thin, wrinkled shell 
that's flattened toward the pointy 
end. If it bumps against the first egg, 
the shell may crack. 

Egg shape is inherited, so you can 
expect to see family similarities. Oc- 
casional variadons are normal, and 
so are seasonal variations. Shells will 
be thicker and stronger in winter, 
but will get thinner in warm weather 
due to a reduction in calcium mobi- 
lization. Soft-shelled eggs are 
common when production peaks in 

A hen lays best during her first 
and second year. Thereafter, as long 
as she is healthy she will continue to 
lay, but not efficiently enough for 
commercial production. Regardless 
of a hen's age, the number of eggs 
she lays, their size, shape, and inter- 
nal quality, and shell color, texture, 
and strength can be affected by a 
variety of things including environ- 
mental stress, improper nutrition, 
medications, vaccinations, para- 
sites, and disease. 

Reproductive Disorders 

Soft-shelled, thin-shelled, or misshapen eggs, ruptured yolks within eggs, re- 
duced production, and prolapse may be [he result of either poor nutrition or 
infection. Watery whites and weak or misshapen shells with altered texture 
and strength can be caused by a viral respiratory disease, such as infectious 
bronchitis or Newcasde, or sometimes by vaccination. A coccidiostat in a 
hen's rations may alter egg size, color, and shell texture. 

Tumors occur in the reproductive organs of hens more often than in any 
other animal and are a common cause of poor laying. Some tumors have 
known causes — notably lymphoid leukosis and Marek's disease — others do 
not. Slow-growing tumors occuring in older hens are understood least of all, 
since only young hens are kept in commercial flocks that sponsor most of the 

Anatomy of a Chicken 53 

Wrinkled and 
misshapen eggs 

Prolapsed oviduct, also called "blowout" or "pickout," is a condition in 
which the lower part of a hen's oviduct turns inside out and protrudes through 
the vent. Prolapse occurs most often when a hen starts laying at too young an 
age, is too fat, or lays unusually large eggs. Caught in time, the prolapse can 
sometimes be reversed by applying a hemorrhoidal cream (such as Prepara- 
tion H) and isolating die hen until she improves. Otherwise, the other chickens 
will pick at her vent, eventually pulling out her oviduct and intestines and 
causing the hen to die from hemorrhage and shock. Not all vent picking is due 
to prolapse, but instead may result from faulty management — feeders, water- 
ers, and roosts may be positioned in such a way that birds below can pick at the 
vents of birds above. 

A false layer is a hen whose egg-laying mechanism malfunctions due to 
damage in chickhood, usually by infectious bronchitis. The hen acts normal, 
visits the nest regularly, but leaves no egg. Instead, yolks drop into die hen's 
abdominal cavity and are partially reabsorbed by the hen's body. A postmor- 
tem examination (see Chapter 1 0) of a false layer will reveal large quant ities of 
orange fat in the body and coagulated, cooked-looking yolk in the abdominal 
cavity. The latter is called "yolk peritonitis" and can be caused, as well, by a 
variety of bacterial infections. 

An internal layeris a hen widi partially or fully formed eggs in her abdomi- 
nal cavity, caused by reverse peristaltic action (die rhythmic, wavelike motion 
that moves an egg through the oviduct). No one knows what causes peristaltic 
action to reverse, and no treatment is known. An internal layer is easily recog- 
nized by her lowered rear end, causing her to stand like a penguin. 

Salpingitis, or inflammation of the oviduct, derives its name from the 
Greek word "Salpinx," meaning trumpet — the shape of the oviduct. 
Salpingids is the most common cause of death in layers. It usually results from 
a respiratory infection, in which bacteria invade the oviduct via one of the ab- 

54 Tun Chicken Health Handbook 

Egg Binding 

An egg travels down the oviduct pointed end first. When it gets to the urogenital 
chamber of the cloaca, it turns end for end so it will come out large end first. 
Sometimes an egg gets stuck. The egg may be too large (for example, if a pullet 
lays unusually large eggs), or a disease may cause the oviduct to swell or its 
muscles to become partially paralyzed. The stuck egg then causes future eggs to 
accumulate behind it, distending thehen'sabdomen. Unless youcan get things 
moving again, the hen will die. 

Lubricate a forefinger with mineral oil or KY Jelly and insert it into the 
vent. With your other hand, push gently against the hen's abdomen to force the 
egg toward the vent. If you can see the egg, but it is too big to pass through the 
vent, puncture the shell and remove it in pieces (with great care not to let a sharp 
shard injure the hen). Rinse the cloaca with hydrogen peroxide. 

through the vent. In that case, protect the hen from cannibalism by isolating 
her until her muscle tone is back to normal. 

dominal air sacs. Most hens die within 6 mondis of becoming infected; survi- 
vors do not lay. If you conduct a postmortem on such a hen, you will find a 
cheesy mass in the oviduct. The longer the infection has gone on, die bigger 
(he mass will be. 

Atrophy of the ovary can occur due to disease or to severe stress caused by 
lack of feed or water. Symptoms, in addition to cessation of laying, are emacia- 
tion and dehydration accompanied by a neck or body molt. 

Spontaneous sex change is a phenomenon whereby an old hen develops 

treated, the "cock" will revert back to a hen at the next molt. If the infection is 
cured before the next molt, the "cock" will lay eggs. This phenomenon was 
once considered witchcraft, the most famous case being a "cock" named Basel 
who was burned at the stake in 1474 for laying eggs. 

• the central nervous system, responsible for voluntary movements 
(like eating) 

tissue may protrude 

Nervous System 

trk coordinating all the other systems. It con- 

Anatomy of a Chicken 55 

• the peripheral nervous system, responsible for involuntary body 
functions (like breathing) 

The nervous system can be disrupted by poisoning (as in the case of botu- 
lism), by a virus (such as die herpes virus causing Marek's disease), or by a 
hereditary defect (such as die recessive genetic trait that causes congenital 
tremor). Typical symptoms of a nervous disorder are incoordination, trem- 
bling, twitching, staggering, circling, neck twisting, convulsions, and paralysis 
of a wing, leg, or the entire body. 

Circulatory System 

Blood type influences a chicken's resistance to disease, alien's egg production 
and vigor, and the hatchability of her eggs. A chicken may have one of twelve 
blood types: A, B, C, D, E, H, % J, K, L, P, and R, which explains why certain 
breeds and strains are more vigorous and less susceptible to disease than oth- 
ers. The resistance factor B21, for example, is found in birds that are immune 
to Marek's disease. 

Blood is part of die circulatory system, which includes the heart and a net- 
work of blood vessels. The heart is a pump that keeps blood circulating 
through the vessels. The function of the circulatory system is to transport oxy- 
gen, hormones, and nutrients throughout the body, but it can also transport 
disease-causing microbes. 

The blood may be invaded by bacteria, viruses, fungi, protozoa, and other 
parasites that get into die blood through mucous membranes or dirough the 
skin, introduced by wounds or insect bites. Some species of parasitic worms 

in which they will grow to maturity. 

Septicemia occurs when any infectious organism enters die bloodstream 
and becomes "generalized" or "systemic" by invading the whole body. Typical 
symptoms that a disease has gone septicemic are weakness, lisdessness, lack 
of appetite, chills, fever, and prostration. In acute septicemia, chickens that are 

a good indication of acute septicemia, since any other fatal condition is likely 
to cause loss of appetite. 

Anemia, or "going light," is a condition in which the blood is deficient in 
quantity (blood loss) or quality (low hemoglobin, red blood cell count, or 
both) . Anemia may be caused by dietary iron deficiency, worms, bloodsucking 
parasites (mites and lice), coccidiosis, and some infectious diseases — notably 
infectious anemia, caused by a virus known as "chicken anemia agent." Signs 
of anemia include pale skin and mucous membranes, loss of energy, loss of 
weight, and death. 

56 The Chicken Health Handbook 


Disorders by the Body System They Affect 




Necrotic dermatitis 
Pox (dry) 










Crop impaction 

Necrotic enteritis 

Newcastle (exotic) 


Pasted Vent 


RotaviraJ enteritis 


Infectious stunting 


Ulcerative enteritis 


Egg drop syndrome 

Joint and Bone 
Cage fatigue 
Gout (articular) 
Infectious synovitis 
Kinky back 

Twisted leg 


Air-sac disease 

Chronic respiratory 

El ukes 
Infectious bronchitis 

Infectious synovitis 


Pox (wet) 

Roup (nutritional) 

Swollen head syndrome 

Blood and 



Infectious anemia 




Algae poisoning 

Congenital tremor 
Epidemic tremor 
Marek's disease 
Newcastle disease 

(Entire Body) 







Chronic respiratory 

Infectious bursal disease 
Infectious stunting 


Lymphoid leukosis 

Marek's disease 

Newcastle disease 




Runting syndrome 







Anatomy of a Chicki-:n 57 

Temperature Control 

A second function of die circulatory system is to aid in regulating body tem- 
perature. The normal body functions of a chicken depend on a relatively 
steady temperature of just under 107°F (42°C). 

A chicken's temperature normally decreases slightly at night and during 
cool weather. Heat is lost through droppings, evaporation (primarily from the 
lungs), conduction (sitting on a cool surface), and radiation (heat lost to sur- 
rounding air that is appreciably cooler than the bird). In an infection that 
causes fever, a drop in body temperature to below normal means death is near. 

Body heat normally increases slightly during the day and in warm 
weather. A rise in body heat also occurs naturally during physical activity and 
digestion. Fever is a symptom of certain infections, including influenza, infec- 
tious bursal disease, and spirochetosis, and any infection that becomes 

General Symptoms of Systems Diseases 

Enteritis: diarrhea, increased thirst, dehydration, loss of appetite, weakness, 
weight loss or slow growth 

Nervous Disorder: incoordination, trembling, twitching, staggering, circling, 
neck twisting, convulsions, paralysis 

Respiratory Disease: labored breathing, coughing, sneezing, sniffling, gasping, 
runny eyes and nose 

Septicemia: weakness, listlessness, lack of appetite, chills, fever, prostration 

Acute Septicemia: sudden death in an apparently healthy bird in good flesh with 
a full crop 

External Parasites 

A PARASITE IS A LIVING ORGANISM that invades the body of another living 
organism and survives without providing benefit. Any living thing ihat invades 
a chicken's body and produces an infectious disease is, by definition, a para- 
site. Those organisms commonly called parasites, however, have certain 
characteristics that set diem apart from other infectious agents. 

• They are animals, while other infectious agents are primitive plant 

• They primarily cause mechanical damage to die body, rather then 
poisoning the body with toxins, as do other infectious agents. 

• They normally cause a long-term decline in health, rather than the 
usual brief life-or-death struggle triggered by other infectious agents. 

Parasites are divided into two groups: internal parasites that invade the 
internal organs (discussed in the next two chapters), and external parasites 
that generally stay on the outside of a chicken's body. 

External parasites, in turn, are divided into two groups: insects (bugs, 
fleas, flies, lice) and mites (cliiggers, mites, ticks). Most external parasites pro- 
duce similar results: weight loss or slow growth, reduced egg production, and 
aesthetic damage to meat birds. Serious infestations may cause deadi, particu- 
larly to young birds. Some parasites carry diseases from one bird to anotiier. 


External Parasites 59 

Chart 4-1 

Diseases Spread by External Parasites 
Disease Transmitted by Disease Transmitted by 


shaft louse 

Marek's disease 

darkling beede 


fowl ticks 



Epidemic tremor 

fowl ticks 


fowl ticks 



Variety of bacterial 






Bugs, fleas, flies, and lice all belong to class Insecta. They all have three-part 
bodies and three pairs of legs attached to the middle part. They develop to 
maturity in stages, and young insects do not look like mature ones. 

Most insects spend at least part of their lives off the bird's body, making it 
possible to control diem by eliminating their favorite hiding places and breed- 
ing grounds — cracks and crevices inside buildings, junk piles outside. 


Bugs are flat-bodied insects belonging to the family Cimicidae, order 
Hemiptera. They all bile to get a blood meal. In doing so, diey inject saliva that 
causes itching and swelling. 

The poultry bug (Haematosiphon modoru) — also called "adobe bug," 
"curuco," or "Mexican chicken bug" — occurs in southern and western states. 
It attacks humans as well as chickens. 

The swallow bug (Oeciacus vicarius) is spread to poultry flocks by barn 
swallows. It has a fierce bite and, like the poultry bug, attacks humans. 

The cone-nose assassin bug (Triatonia sanguisiiga in California, Florida, 
Maryland, and Texas, T. protrata in California and Utah) bodiers chickens but 
is a relatively minor pest. 


The most common bug diat affects chickens is 
the bedbug (Cirnex leclidarius in temperate areas, 
C. boueti and C. hemipteriis in the tropics and sub- 
tropics). This bloodsucking parasite is so 
well-known for attacking humans that it is men- 
tioned in an old nursery rhyme ending witii the line, 
"Don't let the bedbugs bite." 

The bedbug infests cracks, crevices, and litter, 
where it can survive for as long as a year without a 

60 The Ci HGKEN Health Handbook 

Life cycle of the Darkling Beetle 
fAlphatobius diapernus) 


Darkling Beetle 

The darkling beetle (Alphalobius 
diaperimis) and its larvae, the lesser 
mealworm, are not, strictly speak- 
ing, parasites of chickens, but they're 
often found in and around poultry 
houses. This beetle is about '/i inch 
(0.5 cm) long and likes to bide in 
corners and under feeders. It is diffi- 
cult to control unless you can take 
advantage of its extreme sensitivity 
to low temperatures: if the tempera- 
ture falls below 40"F (8"C), thor- 
oughly clean out the coop and open 
it up to the chill. 

blood meal. It feeds at night, for 
about 10 minutes at a lime, and is 
rarely seen on birds during the day. 
Evidence of bedbug infestation is 
black fecal spots deposited on eggs 
and in cracks, and the characteristic 
unpleasant odor created by the 
bugs' stink glands. 

Adult bedbugs are up to V* inch 
(0.5 cm) long. The female lays sev- 
eral eggs per day until she has 
produced between 70 and 200 eggs. 
Depending on the temperature, the 
eggs hatch in 6 to 17 days. In 1 to 3 
months, again depending on tem- 
perature, young bedbugs go 
through several stages to reach ma- 
turity and begin reproducing. 
Control includes removing infested 
litter, cleaning oul housing, and 

insecticide approved for poultry. 

Fleas are insects (order Siphon - 
aptera) with an enlarged third pair 
of legs that allow them to jump. 
They spend most of their lives off 
their host, usually in bedding or 
grass. They live for weeks off the 
host, but survive for up to a year if 
they temporarily return for a blood feeding. Females lay several eggs per day, 
which hatch in bedding, litter, or grass. 

Most fleas are brown and are large enough to see with the naked eye. They 
are particularly abundant in temperate and warm climates. Of the six species 
that attack poultry, three are important in North America. 

The European chick flea (Ceratophyllusgallinae) is most likely to be found 
in northeastern areas. It lives in nests and litter, and stays on birds only long 
enough for a blood meal. 

The western hen flea (C. niger) is common along the Pacific Coast and 
northward into Alberta. It is similar to the European chick flea, but occurs in a 


External Parasites 61 


Sticktight Fleas 

The sticklight flea (Bchtdnophaga galliiiacea) — 
also called "southern chicken Ilea" or "tropical hen 
flea" — is quite common all across the southern 
United States and as far north as New York. It is par- 
ticularly prevalent in sandy areas. 

The tiny, reddish brown tleas measuring %ofl of 

Sticklight Flea 

as well as chickens. They attach themselves in clus- 
ters of 100 or more to the skin of a chicken's head, 
where they remain For weeks. Sometimes they imbed 
their mouths permanently into the skin to suck the chicken's blood. The re- 
sulting blood loss may cause deadi, especially to young birds. 

Sticktight fleas are easy to control on birds using a flea salve or poultry- 
approved insecticide. Unfortunately, they are difficult to remove from 
housing, due to die female's habit of forcefully ejecting eggs so they will lodge 
and hatch in sand or litter. Control involves removing infested litter and 

two or three times at 1 0- to 1 4-day intervals to kill fleas that hatch in the mean- 

Sunlight, heat, excessive moisture, and freezing all inhibit sticktight and 
other fleas. Moisture may be used to control fleas when housing is empty be- 
tween flocks. Sunlight, heat, or cold may be used effectively in a clean coop 
that can be opened up for complete exposure. 

Flies are insects of the order Diptera, meaning "two-winged." One pair of 
wings is for flying, the other is for balance. Flies that bother chickens fall into 
two categories: biting flies and filth flies. Both kinds spread diseases and para- 
sitic infections. 

Biting Flies 

Biting flies are found primarily around bodies of water. The two main 
kinds that bother chickens are black flies and biting gnats. 

Blackflies (Simulium spp) — also called "buffalo gnats" or "turkey gnats" 
— are found at the edge of flowing water. They are approximately the same size 
as mosquitoes, but are chunkier and have rounded or humped backs. They 
transmit leucocytozoonosis and sometimes attack in swarms large enough to 

62 The Chicken Health Handbook 

cause anemia and death. 

Blackflies are difficult to control. Your best bet is to 
control larvae in spring (using an insecticide locally 
approved for ihe purpose), before adults emerge. 
Chickens kept in strict confinement may be pro- 
tected from blackflies by windows fitted with 
fine-mesh screens. 

Biting gnats (Culicoides spp) — also called 
i," "no-see-ums," "punkies," or "sandflies" — are found in swampy ar- 
eas. Attacks irritate chickens, causing them to become restless and to eat less. 
Like blackflies, biting gnats are difficult to control. A good start is to eliminate 
sources of stagnant water. 

(Simulium spp) 

Filth Flies 

The common house fly (Musca domestica) and odier filth-breeding flies 
don't bite, but they irritate birds, transmit tapeworm (by ingesting tapeworm 
eggs diat infect a chicken when it eats die fly), and spread bacterial diseases. 
Flies also leave annoying specks on eggs, and they bother neighbors, some- 
times leading to nuisance-abatement lawsuits. 

Fly problems are a direct result of housing a flock in an artificial environ- 
ment without providing proper management. Flies breed in damp litter and 
manure. An important fly-control measure is keeping litter dry by guarding 
against leaky waterers, leaky roofs, and run-off seepage due to improper grad- 
ing outside. 

Good ventilation also helps dry out ma 
, a ceiling fan not or 

ife cycle of House Fly 
" \usca domestical 






External Parasites 63 

Homemade Fly Trap 

How many traps you need de- 
pendson howbigyourchicken 
house is and on how bad the fly 
problem is.'U 
need a milk jug or similar con- 
tainer. Cut four 3-inch (6 cm) 
diameter holes into the upper 
one-third of the jug, one hole 
in each face. In the bottom of 
the jug, place 2 tablespoons of 
commercial fly bait granules 
containing the fly sex phero- 
mone (common brand names 
include Muscalure and Tri- 
colure). Hang the jug close to 
the ceiling. Flies will enter the 
jug to feed on the bait and die 
before they can leave. As dead 
flies accumulate, replace the 
i a new one. 

flies from bothering chickens. 

A common mistake that can lead to a 
warm-weather population explosion of 
flies is to remove litter without thor- 
oughly cleaning the coop. When manure 
accumulates and dries out, it attracts fly 
parasites and predators that naturally 
control flies. If you remove litter and ma- 
nure, you also remove the natural fly 

Letting manure accumulate during 
warm weather, and making sure it stays 
dry, is a good fly-control method. An- 
other is cleaning out litter and manure at 
least once a week. The cleaning must be 
absolutely thorough — one small clump 
of manure contains enough fly eggs to 
produce hundreds of flies. Dispose of the 
litter by composting it, burying it, or 
spreading it on a field where chickens 
won't roam within the next year. 

If Hies get out of hand, avoid using 
insecticides or you'll run the risk of 
breeding a resistant fly population. One 

alternative is to introduce fly predators, purchased from one of several mail- 
order sources. Another alternative is to buy or make fly traps. 


The occasional mosquito does not seriously bother a chicken, but a mass 
attack lowers egg production and can cause deadi. Several mosquito species 
(Aedes and Culex spp) transmit poultry diseases, including malaria and pox. 
Such diseases are most likely to occur in late summer and early fall, when cool 
nights attract mosquitoes to the warmth and lights of a poultry house. 

Control mosquitoes by eliminating their principal breeding grounds — 
stagnant water in persistent puddles, old tires, and swampy areas. Where 
mosquitoes are dense, vaccinate against pox. 


Lice come in two varieties: blood-sucking and chewing. Bloodsucking lice 
attack only mammals. Chewing or biting lice (order Mallophaga) attack both 

64 The Chicken Health Handbook 

mammals and birds. Several species infest chickens, and a bird may be in- 
fected by more than one species at a lime. 

Lice are species specific, meaning a louse that prefers chickens doesn't like 
any other kind of bird or animal. How seriously chickens become louse- 
infested, or lousy, depends in part on their strain — some strains are more 
resistant than others. Debeaked birds, because they can't groom properly, are 
more likely to become seriously infested than other chickens. 

An infested bird becomes so irritated from being chewed on that it doesn't 
eat or sleep well. Egg production may drop as much as 1 5 percent, and fertility 
may also drop. Chickens get restless and injure themselves by scratching and 
pecking dieir own bodies. In the process, feathers get damaged — an impor- 
tant consideration if the birds are raised for show. In a serious infestation, 
especially in chicks, birds die. 

Louse infestation (technically called "pediculosis") often accompanies 
poor management and associated problems such as malnourishment, inter- 
nal parasites, and other infections. Whether louse infestation causes these 
problems, or these other problems make chickens more susceptible to lice, is 
arguable but entirely academic. 

Lice Species 

Lice species vary in shape and size, ranging in length from His to Yt inch (1 
to 5 mm) — big enough to see with the naked eye. Most lice 
are yellow or straw-colored, making them difficult to see 
on white chickens, but easy to spot on dark-feathered vari- 

Among the different species that attack chickens, each 
has a preference for feeding on certain parts of the body, 
resulting in descriptive common names such as wing 
louse, head louse, and fluff louse. Most lice eat feathers, 
skin scales, and odier organic matter on the skin. An ex- 
ception is the body louse, which chews through skin and 
punctures growing quills to get blood. Body and head lice 
are the two most serious louse pests of poultry. 

In a heavy infestation of body lice (Menacanthus 
stramineus), you'll find numerous scabs on the bird's skin 
and pearl-colored egg masses at die base of feathers. Body 
lice move fast — when you part a bird's feathers, take a 

The head louse (Cuclotogaster lieterogmpluts) is the 
most serious louse pest of young birds, particularly in 
heavily featiiered breeds like Polish and Cochin. It spreads 
from a hen to her chicks, causing the little guys to become 

Head Louse 

Body Louse 

External Parasites 65 

Common Name 
Scientific Name 

Body Pari 




of Louse 


in North 

head louse 


head and 

base of 

oblong, grayish, 
0.1" (2.5 mm) 

to down or 
leather base 


small body louse 





under wings 

close to 

like body 
louse, but 

like body 
louse eggs, 
but smaller 


body louse 

M. stramineus 

vent, breasi, 

under wings 

close to 
skin in 


in clusters 
near feather 


small body louse 

M. paltidulus 

vent, breasi, 

under wings 

close to 

like body 
louse, but 

like body 
louse eggs, 
but smaller 


shaft louse 




like body 
louse, but 
and paler 

in strings 
on feathers 


wing louse 

Lipewus caponis 


wing, tail, 
back, and 

slender, gray, 
moves slowly 

in clusters 

feather base 


fluff louse 


body feather 

and vent 

small, broad, 
yellow, slow 

in clusters 
near feather 


large chicken 

Goniodes gigas 

body and 



smokey gray 
0.25" (5 mm) long 

in clusters 
near feather 


brown chicken 

G. dissimilis 






in clusters 
near feather 


66 The Chicken Health Handbook 

1 month 

of age. 

The shaft louse (Menopon gallinae), which does not infest young birds 
until they become well feathered, is a possible transmitter of chlamydiosis. It 
punctures soft feather quills near the base and leaves strings of light-colored 
eggs on feadiers. It likes to rest on feadier shafts, but scurries toward the bird's 
skin when you part the feathers. 

The fluff louse (Goniocotes gallinae) is fairly common. It stays mainly on 
fluff and is relatively inactive, so it causes little irritation or injury. Similarly, the 
brown chicken louse (Goniodes dissimilis) which occurs primarily in the 
South, lives on body feadiers. Two species of small body lice (Menacanthus 
cornutus and M. pallididus) are similar to each other, and both are often mis- 
taken for immature body lice. These and odier lice species are not particularly 
common in North America. 

Life Cycle and Treatment 

A louse lives for several months, going through its entire life cycle on a 
bird's body. It can survive less than a week off die body. The female louse lays 
her eggs, called "nits," on a chicken's feathers and makes sure they stay there 
by sticking them down with glue. 

Nits hatch in 4 to 7 days. Young lice, called "nymphs," are unlike other 
insects in that they look like adults, only they're smaller and nearly transpar- 
ent. They go through several molts and develop color as they grow. 

When a louse matures, it mates on the bird and starts laying nits. One fe- 
male may lay as many as 300 nits in her lifetime. Since lice go through one 
generation in about 3 weeks, in just a few months one pair explodes into 

Lice usually travel to chickens by way of wild birds or used equipment. 
They spread by crawling from bird to bird or through contact with infested 
feathers, especially during a molt. 

Lousiness is usually worse in fall and winter. Suspect lice if your chickens 
are restless and constantly scratch and pick diemselves. Look for moving lice 
on feathers and skin, and for white or grayish egg clusters at the base of feath- 
ers. If you see lice on one bird, chances are good the whole flock has them, or 
soon will. 

Inspect your birds at least once a month. As soon as you spot lice, treat the 
flock by spraying or dusting with an insecticide approved for poultry. Spray 
caged birds from the bottom as well as from the sides and top. Treat litter- 
reared birds by sprinkling powder on the litter and in preferred dusting areas. 
Treat individual birds by placing a pinch of powder beneadi each wing and in 
the vent area. For head lice, mix insecticide powder with Vaseline and rub it on 

External Parasites 67 

each bird's head and neck. Since no insecticide kills nits, repeat the treatment 
twice at 7-day intervals. 

Mites belong to the tribe Arthropoda, characterized by exterior skeletons and 
jointed limbs. They are members of die class Arachnida, a group of spider-like 
creatures with single-segmented bodies and four pairs of legs. 

Mites are quite small, usually under V2S inch (1 mm) in 
length; some are microscopic. All have mouths designed for 
piercing or chewing. Depending on the species, they live on 
blood, tissue cells, or feathers. 

Most mites spend a lot of time off the bird and are spread 
by contaminated equipment, shoes, or clothing. They are also 
spread by infested birds, including wild ones. 

Some mites remain on a chicken's skin. Others hide in 
feather parts, burrow under the skin, or make their way deep 
within the body to live in the lungs, liver, or other organs. Mite 
infestation (technically called "acariasis") causes irritation, 
low vitality, plumage damage, increased appetite accompanied by low egg 
production, reduced fertility, retarded growth in young birds, and sometimes 
anemia and deatii. 

Red Mite 

Red Mites 

The red mite (Dermanyssus gal'inae) — also called "chicken mite," "poul- 
try mite," or "roost mite" — is the most common mite found in warm climates 
and is a bigger problem in summer than in winter, since it becomes inactive 
when the temperature drops. The red mite is more likely to be found on litter- 
raised birds than on those kept in cages. 

Red mites are grey until they suck a chicken's blood and turn red. They live 
and lay their eggs in cracks near roosts or nests. They survive for up to 6 
months off chickens, so housing may remain infested long after chickens have 
been removed. 

The red mite population increases rapidly in hot weather; one female lays 
as many as 120,000 eggs. The mites feed at night. In a heavy infestation, some 
mites may stay on birds during die day and can kill chicks and setting hens. In 
a particularly severe infestation, red mites invade the roof of a bird's mouth, 
causing serious anemia. Red mites, when abundant, will also attack humans. 

Check birds at night, when mites are on the prowl. You'll see little specks 
crawling on the roost or on the birds themselves. Red mites can be controlled 
solely by cleaning up the birds' environment — no need to treat individual 

68 The Chicken Health Handbook 

Chart 4-3 






in North 






.SnrrnnI idnt* 







part of legs 

K. gaUinae 


in skin at base 



of feathers 




body and upper 




legs on birds 




eating mite 


Cylodites nudus 

air-sac mite 





I i i i 1 i ; 1 ' i M r : 1 

L-ySl unit 

i i ii Hf> r cL'i n 
UM'.H ! - !• . i ! 

I I ii L"T*i niA/n 

III 1 M It! Wl I 



tp^tnci* milt* 
it- it ii ii i Hint. 

ll_llO (1111.1 1 IL.C1U 


til II 1/ (If f ClL- 

A'/ i'i/hi ff/Iis 

I'll lid tA 

fp;i t hpr mil p 

ICil LI II- 1 1 1 1 1 II. 

mi liirHs 

U 1 1 17 1 1 LI O 



quill mite 

inside quills 



D. elongalus 

quill mite 

inside quills 


feather mite 

on flight and 

tail feathers 

Kill J 


Aconuttacartis galli 


hedgerows and 


Nsoschnnpeifitl n 

i Wv^wOCJ J IS f 1 OH LI* 


dens. 1 brush 


HifiCt 11(11111 

rh ipppr 

Tfft m ■tir'i il fi 
1 1 ullUtLtlltl 

n ITFPtl/l 1 1 HP 9 / 

Hlj 1 l Lilt 1 1 LCOI 

I . UUIUtllit 


7 wilt*Hfiens 

red bug 



quill mite 

inside quills 



lit* irnfl n tnsc i/l n/" 

TiBPntfm\lBtttt c 

ron ni i li» 

1 CU 1111 IL 

at night in nests 



and cracks; during 

day on birds 



on birds 



fowl mile 


O. bursa 

tropical fowl 

on birds 






fowl tick 

wood litter, cracks 




lone star 

wood litter, cracks 






A. maculatum 

Gulf Coast 

wood litter, cracks 













External Parasites 69 

birds. Clean facilities thoroughly and dust with a pesticide powder approved 
for poultry, with particular attention to cracks and crevices. Repeat the dusting 
in 5 to 7 days. 

Fowl Mites 

The Northern fowl mite (Omithonyssus sylvia- 
rum) is the most serious external parasite of 
chickens and the most common one found in cooler 
climates. It completes its entire life cycle in less than 
a week, so an infestation worsens rapidly. In con- 
trast to red mites, Northern fowl mites increase 
more rapidly in cold weather. 

This mite differs from the red mite in another 
way — it survives only about a month off the bird. It 
lives its entire life on the bird and therefore does 
more damage than the red mite. 

Evidence that northern fowl mites are present 
includes mites crawling on eggs in nests, large num- 
bers of mites on the skin of birds during die day, 
darkened vent feadiers, and blackened, scabby skin 
around the vent. This mite moves quickly and will 
crawl up your arms when you handle your chickens. 
Control involves dusting individual birds with a pes- 
ticide approved for poultry. Repeat the dusting 
again in 5 to 7 days. 

The tropical fowl mite (Omithonyssus bursa) re- 
sembles the northern fowl mite and seems to 
replace it in warm areas. Like the northern fowl mile, the tropical mite lives its 
entire life on the bird, but by contrast is more likely to lay eggs in poultry nests. 
Control involves dusting nests as well as individual birds. 

Skin Mites 

The scaly-leg mite (Knemidocoptes /nutans) is a pale gray, round, tiny 
creature, only about Viao of an inch (0.5 mm) in diameter. It is more likely to 
attack older birds, but also affects young birds kept with old birds. It burrows 
into the unfeathered portion of the skin on a chicken's shanks, raising the 
scales by generating debris that accumulates beneath them. As a result, the 
legs diicken and crust over. In severe infestations, this mite attacks combs and 
wattles as well as legs. 

The scaly-leg mite spends its entire life on the chicken. Once it invades, 

Northern Fowl Mile 
sylviarum) found in cool 

Nearly identical Tropical 
Fowl Mite (Omithonyssus 
bursa) found in warmer 

70 The Chicken Health Handbook 

Controlling Scaly-Leg Mites 

Scaly-leg mites spread slowly by traveling from bird to bird. They can be 
controlled by brushing perches and chickens' legs once a month with a mixture 
of one part kerosene to two parts linseed oil (not motor oil). 

Scaly-leg and other burrowing miles can be controlled in exhibition birds 
with ivermectin (trade name Ivomec), an over-the-counter cattle wormer sold 
at most feed stores. Give a bantam 5 to 7 drops by mouth; give a larger bird V* cc 
by mouth. Since the withdrawal time is not known, ivermectin should not be 
used on birds kept for meat or eggs. 

you'll have a hard time getting rid of it. The best approach is to cull affected 
birds. Treatment involves smothering the mites by applying a kerosene- 
linseed oil mixture (see box) to the chicken's legs every 10 days until the 
problem clears up. Coat the legs with mineral oil or warmed petroleum jelly 
(Vaseline) to loosen old, crusty scales, but don't expect raised scales to return 
to normal. 

Scaly-skin mite (Epidermoptes bilobatiis) is a relatively rare parasite that 
causes avian scabies. The mite burrows into the skin of a chicken's body and 
thighs, causing inflammation and itchiness. The skin thickens with brownish- 
yellow scabs that may become infected with fungus. A serious infestation 
causes emaciation and death. The scaly-skin mite is difficult to control. Keep it 
from spreading by isolating or culling infested birds. 

Feather Mites 

Feather mites live on and eat plumage, ruining feathers by chewing stripes 
across them or by damaging the feather base. Luckily, these mites are not com- 
mon in North America. 

Perhaps the most common among them is the depluming mite 

External Parasites 7 1 

(Knemidocoptesgallinae), a tiny creature that is barely visible to the naked eye. 
It burrows into tire skin at the base of feathers, causing the chicken to scratch 

spread. Treatment involves dipping individual birds in a solution made up of 1 
ounce (30 grams) soap, 2 ounces (60 grams) sulfur, and 1 gallon (4 liters) warm 

The quill mite (Syringophtttii bipectinatiis) inhabits a feather quill, result- 
ing in partial or total loss of the feather. Evidence of its presence is die powdery 
residue it leaves in the quill stump. Since these mites hide inside feathers, the 

only known way to control them is to dispose of affected birds and thoroughly 
clean their housing. Quill mites occur in the eastern states, but are quite rare. 

• the feather-eating mite (Rivoltasia bifurcata), which does little damage 

• the Canadian feather mite (Megiiinia gallinulae), which causes crusty 
heads and the loss of leg scales 

• the southern feather mite (M. cubitalis), which is similar to the Cana- 
dian feather mite but occurs primarily in the southern United States. 

Internal Mites 

Although mites are basically external parasites, they sometimes invade the 
inside of a chicken's body, either by burrowing under the skin or by invading 
internal organs. No one knows how common they are. Since diey do not cause 
serious health problems, few people look for them. As a result, little is known 
about them. 

The cyst mite (Laminosioptes cysticola) — also called "flesh mite" or "sub- 
cutaneous mite" — is a tiny creature visible only under a microscope. It 
burrows into a chicken's skin, where it does little damage until it dies. Then it 
becomes encased in a yellowish nodule (somewhat resembling a nodule 
caused by tuberculosis). The main problem cyst mites cause is destroying the 
aesthetic appeal of meat birds. The only known way to get rid of them is to 
destroy infected birds. 

The air-sac mite (Cytodites nudus) invades a chicken's respiratory system, 
where it seems to do little damage unless it becomes abundant. A serious infes- 
tation produces symptoms that resemble avian tuberculosis: emaciation, 
anemia, and death. During postmortem examination (see chapter 10), you can 
see the mites as slow-moving white dots on die air-sac surfaces. The only 
known method of control is to cull affected birds. Unlike other mites, which 
hatch from eggs and molt several times to reach maturity, air-sac mites are 
born live and spend their entire life cycles in a chicken's windpipe, lungs, air 

Also rare are: 

72 Tim Chicken Health Handbook 

Chigger mites — also called "jiggers," "harvest mites," and "red bugs" — 
infest the skin of birds, humans, and other animals. Of the 700 known species, 
only 4 are common in the United States and Canada. Chiggers are most preva- 
lent east of the Rockies, although some species occur in Arizona and 
California. The adult, identified by its red, figure-eight 
shaped body, feeds on plants. Only the larval stage is 
parasitic. In southern slates chiggers go through several 
generations per year; in the north, they go through only- 
two or three generations. 

Chigger larvae have diree pairs of legs, instead of the 
usual four of other mite forms. They are about VI50 inch 
(0. 1 7 mm) long — so small they can barely be seen with 
Chigger Mite Larvae the naked eye. They are straw-colored, making them 
(Jfombtcula even more difficult to see until after they feed, when thev 
alfredduges,) , Qok |jke red dots 

Chiggers are fond of attacking a chicken's neck, breast, and wings. They 
pierce the skin with their mouths, inject poisonous saliva that liquifies the skin, 
and feed on liquified skin for up to 6 days before dropping off. The bite causes 

come droopy, stop eating and drinking, and sometimes die. 

Since chiggers prefer tall weeds, they can be a problem for free-ranged 
chickens. The best method of control is to keep weeds mowed around your 
coop. Where chiggers are especially numerous, repel them by dusting or 
spraying with sulfur. 



Trombicula (ilfredclugesi 
T. baiattis 
T. splendeivs 

tropical areas 
eastern U.S. 

grassy meadows, dense brush 

dry, brushy areas 
sunlit, grassy meadows 
swamps, bogs, rotten logs 

Scavenger Mites 

Scavenger mites (family Uropodidae) live in poultry litter and feed on 
fiangi They are especially numerous where new pine shavings are thrown on 

External Parasites 73 

top of old litter. Discovering an infestation of scavenger n 
but don't worry — these mites do not attack chickens. 


Ticks are really nothing more than big mites. They are divided into three 
families, two of which are parasitic — Argasidae or soft ticks and Ixodidae or 
hard ticks. 

Soft Ticks 

Of several species of soft ticks, Argas persicus is the most prevalent in the 
United States. It is commonly known as the "fowl lick," "adobe tick," "blue 
bug," "chicken tick," or "tampan." It mainly occurs in the southwestern states 
and along the Gulf Coast. 

Fowl ticks are leathery, egg-shaped, flattish and up to '/2-inch ( 12 mm) long. 
They feed only on blood and can survive as long as 4 years 
between feedings. They are tan or reddish-brown until they 
feed, then :hey turn bluish. 

A female tick lays as many as seven batches of eggs con- 
taining up to 150 eggs each. She deposits her eggs under tree 

about 10 days; in cool weather, they take up to 3 months. 
Tick larvae crawl around until they find a host, attach them- 
selves, and feed for about a week. They leave the bird to 
molt, then return for another blood meal. 

Ticks are particularly active during dry, warm weather. They hide in cracks 
and crevices during the day and come out at night to feed. Feeding takes 15 to 
30 minutes and leaves red spots on the bird's skin. Chickens that expect to be 
bitten become resdess at roosting time. 

Other signs of infestation are ruffled feathers, weakness, depressed appe- 
tite, weight loss, a drop in laying, and sometimes diarrhea. The bile wound 
may become infected with bacteria. In a growing or mature hen, toxins re- 
leased from the ticks' saliva can cause transient paralysis that is sometimes 
mistaken for botulism or Marek's disease. Soft ricks also spread a number of 
diseases, including cholera, epidemic tremor, and spirochetosis. A large infes- 
tation causes anemia, emaciation, and death. 

Control includes housing chickens in a metal building (to eliminate hiding 
places), and installing suspended roosts or keeping birds in cages (so ticks 
can't easily climb onto them). Eradicating ticks is difficult. It involves thor- 
oughly cleaning housing and spraying with a pesticide labeled for ticks that is 
approved for use with poultry. Use a high-pressure sprayer and pay special 
attention to cracks and crevices. 1 

Fowl Tick 
(Argas persicus) 

74 The Chickkn Hualti i Handbook 

ticks, dipping is more effective than spraying. 

Since ticks molt several times before reaching adulthood, and the entire 
process takes about 8 weeks (longer, in winter), spray every week for at least 8 

one type. 

A serious tick infestation involving the transmission of a disease may re- 
quire such drastic measures as cutting down and burning nearby trees in 
which chickens roost and/or burning down infested housing. Moving tick- 
infested chickens to new housing will, however, only move the problem to a 
new location. 

Hard Ticks 

Hard ticks are most likely to be found on free-ranged chickens in temper- 
ate and tropical climates. Two kinds affect chickens in North America. 

The lone star tick (Amblyoinma americanum) occurs from southern Iowa 
eastward to the Atlantic Coast and southward into Mexico. It is found in wood- 
land and brushy areas, and attacks dogs and humans as well as chickens. Since 
it transmits human diseases, you don't want one of these to 
bite you. 

The adult female lone star tick is pear-shaped and chest- 
nut-brown with a pale spot on her back. Shell lay between 
5,000 and 7,000 eggs, which take 32 days to hatch. The lar- 
vae, called "seed ticks," are straw-colored and crawl 
arotuid in bunches. Nymphs are light to dark tan and are 
smaller than adults. The lone star tick has a 1 -year life cycle, 
during which it feeds three times on three different hosts. 
The Gulf Coast tick {Amblyomma maculatum) is chest- 
nut-brown with colorful patterns on its back. It occurs along the Atlantic Coast 
from Virginia southward into Florida and westward along the Gulf Coast into 
Texas, decreasing in numbers as it moves inland. Although it attacks chickens, 
it prefers humans, dogs, and other large animals. Each female lays 15,000 to 
19,000 eggs, which take 19 to 28 days to hatch. Larvae usually attach them- 
selves to tire neck area and feed in groups. 

Lone Star Tick 

Not all external parasites are equally common in all areas of the country. Your 
state Extension poultry specialist can tell you which parasites are most likely to 
be found in your area and can advise you on currently approved methods for 
their control. 

Many parasites can be controlled through good management, including 

External Parasii BS 75 

giving housing a periodic thorough cleaning. Once parasites invade a coop, 
sometimes the only way to get rid of diem is to use a pest icide. 

Methods for applying pesticides to birds can be divided into two catego- 
ries: individual treatment and flock treatment. Individual treatment is more 
effective, but flock treatment is more practical for a large flock. 

No pesticide destroys parasite eggs. To avoid reinfestation when eggs 

cycle of the parasite involved. 

Pesticide Use 

The list of pesticides recommended for poultry is fairly short and changes often 
due to two things: continuing development of resistant strains of parasites and 
new knowledge about the dangers of various products. Even approved pesti- 
cides are toxic and should be handled with care. Always read die label and follow 
all precautions. 

Before applying any pesticide, remove or cover feeders and waterers and 
gather eggs. Wear gloves and a face mask, and avoid inhaling sprays or dusts. If 
you spill any on yourself, wash your skin and launder your clothing. After 
applying a pesticide, wash your clothing separately. 

Store pesticides away from children, pets, livestock, foods, and feeds. Keep 
them in their original containers with their labels intact. Puncture empty 
containers so they can't be reused. Due to laws regarding toxic wastes, getting 
rid of empty containers can be difficult. Check widi your local waste-disposal 

Some pesticides approved for poultry are restricted, meaning you must 
obtain a permit to use them. Contact your county Extension office or state 
poultry specialist for details. Obviously, your best bet is to avoid using toxic 
chemicals by managing your flock so you don't need them. 

Pyrethnim. One fairly safe natural pesticide is pyredimm, a plant extract 
that's relatively non-toxic to humans and birds but is highly toxic to insects. 
Put into a squeeze bottle and puffed into cracks and crevices, or powdered 
onto vent fluff and beneath wings, it wards off body parasites and flies. 

Dust baths. Old-time poultry keepers controlled external parasites by pro- 
viding their flocks with bins of fine road dust or ashes, sometimes adding sulfur 
or lime-and-sulfur garden dust to enhance the beneficial effects of the dust 
bath. Chickens instinctively dust themselves to keep clean and rid themselves 
of external parasites, which they dislodge by pulling feathers through their 

a trade-off — chickens are highly susceptible to respiratory problems, and in- 


haling exotic materials makes matters worse. 

Nicotine sulfate. Another old-time treatment that works wonderfully well 
is the gardening pesticide nicotine sulfate (sold as a 40 percent solution under 
die trade name Black Leaf-40). It works by evaporating when it is warmed by a 
bird's body heat. It's painted on roosts just before nightfall or dabbed on vent 
fluff. As a 2 percent dust it's puffed into vent feathers. The use of nicotine sul- 
fate on poultry has been banned in some states because it is highly toxic if 
spilled on the skin of chickens (or humans). Old-timers could sometimes re- 
vive a poisoned bird by tossing it into the air, causing the bird to flap its wings 
and inhale oxygen by reflex, but the trick didn't always work and the bird often 

Petroleum oil. A safer old-time method that's messy but effective against 
parasites living off a bird's body is to paint petroleum oil onto roosts and nests 
and into cracks and crevices. It works by coating and smothering lice and 
mites, but can create a fire hazard in a wooden building. 

Dog dip/shampoo. Two odier products that work quite well for chickens 
are flea dips and flea-tick-louse shampoo for dogs. Shampooing is ideal if you 
wash your birds for exhibition anyway. On a warm, sunny day, wash each bird 
in warm water, soaking the bird thoroughly and working a good lather among 
the feadiers. Rinse die bird at least twice in warm water. Pat the feathers dry 
with towels. Let the bird dry in a warm area, away from drafts, or hasten drying 
with a blow dryer. 

Systemic inhibitors. A fairly new idea being developed for chickens is the 
use of systemic inhibitors that minimize infestation by making a chicken's 
body unpleasant to parasites. Commonly used systemic inhibitors include 
brewer's yeast fed to cats to ward off fleas, and vitamin B taken by humans to 
keep mosquitoes away. Some drugs, including the coccidiostat sulfaquin 
oxaline and the catde wormer ivermecdn, work similarly. 


Despite the success of extra-label uses such as those suggested above, it 
isn't a good idea to experiment with products that are not specifically intended 
for poultry unless: a) you do not plan to eat meat or eggs from your flock in the 
near future, and b) you're prepared to lose birds treated widi inappropriate 

Internal Parasites: Worms 

INTERNAL PARASITES ARE DIVIDED into two major categories — protozoa 
(discussed in the next chapter) and the group commonly known as worms. 
Worms can become a problem in ground-reared flocks, particularly where 
chickens are kept in the same place year after year. Most infestations develop 
rather slowly. 

Under good management, worms and chickens become balanced in 
peaceful co-existence. Through gradual exposure, birds can develop resis- 
tance to most parasites. An overload is usually caused by disease or stress. 

If the scale tips in favor of the worms, the chickens may gradually lose 
weight as die worms interfere with food absorption and other digestive pro- 
cesses. Some worms, instead of invading the digestive tract, invade the 
respiratory system, causing breathing difficulties and gradual blockage of air- 
ways. Less common worms invade other parts of the body. 

Worms are divided into two main groups, according to the shapes of their 
bodies. Roundworms or Nemathelminthes have cylindrical bodies; flatworms 
or Platyhelminthes have flattish bodies. In turn, roundworms, are divided into 
two groups, nematodes (also called "roundworms") and acandiocephalans 
(thorny-headed worms). Flatworms are also divided into two groups, cestodes 
(tapeworms) and trematodes (flukes). 


78 The Chicki n HeaiAh Handbook 

Intermediate Host 

Some worms have direct life cycles whereby female worms living in a chicken's 
body shed eggs that pass out of the chicken in droppings and are eaten by the 
same or another chicken to begin a new life cycle. Other worms have an indi- 
rect cycle that requires an intermediate host. A host is any living thing in which 

Indirect Life Cycle of Roundworm or Tapeworm 

Chicken acquires 
parasite by eating 1 r _^,, 
intermediate host '^Ssjffo 

Eggs eaten by 

intermediate host (beetle, ■ ' 

fly, slug, earthworm, t — -"C 
grasshopper, etc.) 

r" Roundworm- or tapeworm-infested chicken 

Roundworm eggs 
or tapeworm 
^'oj?" c containing eggs 
■4$T- & ore passed in 

J ~ 

Topeworm egg 

Internal Parasites: Worms 79 

a parasite resides. In an indirect 
cycle, worm eggs expelled by a 
chicken are eaten by a grasshopper, 
earthworm, or other intermediate 
host. A chicken becomes infected or 
reinfected by eating the intermediate 
host (or being bitten by the interme- 
diate host, which releases parasite 
larvae in its saliva). 

More than half the nematodes 
and all the tapeworms that invade 
chickens require an intermediate 
host. These indirect-cycle parasites 
create greater problems in late summer, when beetles, grasshoppers, and 
other intermediate hosts proliferate. Knowing which parasites have indirect 
life cycles, and which intermediate hosts are involved, is an important part of 
any parasite control program. 

Controlling Worms 

Controlling parasitic, worms requires good management rather than constant 
medication. Not only can parasites become resistant to medication, but 
worming becomes an expensive and never-ending cycle unless you eliminate 
the source of infection. 

Reducing the need for worming medications includes providing a 
proper diet; a diet that's high in vitamins A and B and animal protein en- 
hances immunity to roundworms. Good management involves these 
sensible parasite-control measures: 

• practice good sanitation 

• eliminate intermediate hosts 

• rotate the range of free- ranged 

• avoid mixing chickens of 
different ages 

• don't raise turkeys with chick- 

Most worms spend part of their 
life cycles away from the bird's body, 
offering a good handle on parasite pre- 
vention and control. To avoid 

Parasitic Worms 
of Chickens 

Nemathelminthes (roundworms) 
Nematodes (roundworms) 
Acanthocephalans (thorny- 
headed worms) 

Platyhelminthes (flatworms) 
Cestodes (tapeworms) 
Trematodes (flukes) 

General Symptoms 
of Worm Infestation 

Usual Symptoms 

Pale head (anemia) 
Reduced laying 

Foamy diarrhea 

80 The Chicken Health Handbook 

so chickens can't pick in their own droppings. To avoid indirect-cycle para- 
sites, keep intermediate hosts away from the coop. Take care when using 
insecticides, though, since chickens can be poisoned from eating poisoned in- 
sects. When possible, use an insecticide only in an unoccupied house, then 
thoroughly clean up before introducing a flock. 


A healthy chicken can tolerate a certain amount of parasitic invasion. 
Avoid using a wonner unless parasites cause your chickens to look scrawny 
and scruffy, lose weight, and lay fewer eggs. If worms get out of control and 
reach the point where they begin to affect the chicken's health, you may have 
no choice but to use a wormer. Wormers are more properly called 


Different brands of the following anthelmintics come in varying strengths. Dos- 
ages vary accordingly. Always follow label directions. 

Counmphos (Meldane) is a feed additive approved for large roundworms, 
capillary worms, and cecal worms. Il is not readily available for small-scale use. 
For replacement pullets, 10 to 1 4 days before laying starts coumaphos is added to 
mash at the rate of 0.004 percent. For hens that are already laying, the rate is 0.003 
percent for 14 days. Since coumaphos has cumulative toxic effects, it should not be 
used within 3 weeks of a previous worming. The withdrawal period is 7 days. 

Hygromycin B is a feed additive approved for large roundworms, capillary 
worms, and cecal worms. Il is not readily available for small-scale use. Minute 
amounts are added to mash at a continuous rate of 0.00088-0.001 32 percent. The 
withdrawal period is 7 days. 

Piperazine is a readily available wormer approved for large roundworms. 
Despite its wide safety margin, it is currently under FDA scrutiny and may one day 
be withdrawn for use in chickens. Piperazine is rapidly absorbed and rapidly 
excreted. It acts as a narcotic, weakening and paralyzing adult worms and causing 
them to be expelled from the chicken, live, with a bird's digestive wastes, but 
requires a high concentration to be effective. Piperazine works best as a one-time 
oral dose of 50 to 100 mg per bird. The next most effective method, and one that's 
more practical for large flocks, is to add piperazine water-wormer to the birds' sole 
source of drinking water at the rate of 0. 1 to 0.2 percent (3 ml per gallon) for4 hours. 

Phenothiazine is approved for cecal worms. 1 1 works oidy against cecal worms 
and has a narrow margin of safety, so take care not to exceed the recommended 

Internal Parasitks: Worms 81 

"anthelmintics" (from the Greek words and meaning "against" and helmins 
meaning "worms"). 

How often your chickens need worming, if they need it at ail, depends in 
part on the way your Dock is managed. Chickens on open range may need 
worming more often than confined chickens. Caged chickens need worming 
least often of all. Flocks in warm, humid climates, where intermediate hosts 
are prevalent year-around, are more likely to need worming than flocks in cold 
climates, where intermediate hosts are dormant part of the year. 

To ensure a wormer's effectiveness (especially if you're battling tape- 
worm), withhold feed from the flock for 18 hours before worming. About an 
hour after worming, feed a moist mash, which causes hungry chickens to eat 

Afteryou've used one wormer for a time, parasites will become resistant to 

dosage of 0.05 grams per bird for 1 day only. The withdrawal period is 7 days. 

Drugs not approved for poultry use (withdrawal periods are therefore not 
made public): 

Levamisole, the active ingredient in tetramisole, is effective against a wide 
varietyof nematodes. It actsonaworm's nervous system, paralyzing the worm and 
causing it to be expelled, live, with digestive wastes. Levamisole drench (for oral 
use) is added to water at the rate of 0.03 to 0.06 percent (10ml per gallon) for one 
day only. Levamisole injectable is injected subcutaneously (beneath the skin) one 
time on ly at the rate of 25 mg per 2 pounds of body weigh t (25 mg/ kg) . Levamisole's 
therapeutic effect in treating a variety of infectious diseases is under investigation. 

Thiabendazoleisa rapidly absorbed, rapidly metabolized, rapidly excreted 
wormer used to kill gapeworm and common roundworm. It is less potent than 
more slowly absorbed and excreted products, making a divided dose (adminis- 
tered over a period of time) more effective than a single dose. The dosage rate in 
feed is 0.5 percent for 14 days; individual treatment calls for 75 mg for each 2 
pounds of a bird's weight (75 mg/kg). Due to its extended treatment period, 
thiabendazole is effective against emerging worm larvae as well as adult parasites. 
Since thiabendazole moves through a chicken quickly, the withdrawal time is 
relatively short. 

Mebendazole is based on thiabendazole and is used for spiral stomach 
worm, common roundworm, and diorny-headed worm. The dosage rate is 10 mg 
for each 2 pounds of body weight (10 mg/kg) for 3 days. 

Ivermectin is effective against a wide variety of internal and external para- 
sites (excluding flukes and tapeworm). It can be toxic to chickens in relatively small 
amounts. Given orally, l A cc is enough to worm a large chicken; up to 7 drops will 
worm a bantam. 

82 The Chicken Health Handbook 

it. Resistance takes between eight and ten generations. To minimize the devel- 
opment of resistant strains, avoid always using the same anthelmintic. Don't 
alternate too quickly, though, or the parasites may become resistant to all the 
wormers you use. For maximum benefit, rotate wormers annually. 

In the old days, anthelmintics worked against a narrow range of parasites. 
Today's more potent wormers work against a wider variety of parasites. They 
work in two ways: by interfering with the parasite's feeding pattern (in other 
words, by starving it), or by paralyzing the parasite so it is expelled live in the 
chicken's body wastes. 

A wormer may be administered to chickens in one of two ways: 

• orally (added to feed, water, or given directly by mouth), to be ab- 
sorbed through the digestive tract: 

Either way, the wormer is transported throughout the chicken s body, me- 
tabolized, and eventually excreted. 

Withdrawal Period 

Different wormers require different amounts of time before they disap- 
pear entirely from a bird's body. Each drug approved for use in poultry has an 
established "withdrawal period" —the amount of time it takes before the drug 
no longer shows up in the bird's meat or eggs. The withdrawal period for most 
wormers is 1 week. 

Because an approved drug against a particular parasite isn't always avail- 
able, many flock owners use drugs that are not approved. Such use is 
considered "experimental" (a designation that allows the drug to be used by 
qualified researchers) or "extra label" (a designation that allows veterinarians 
to prescribe die drug as needed). Since no withdrawal period has been estab- 
lished for them, drugs that are not approved should not be used on chickens 
kept for meat or eggs. (Chickens raised for meat reach butchering age so 
quickly that worming them shouldn't actually be necessary.) 

Drug approval keeps changing, so what was "in" today is "out'' tomorrow, 
and vice versa. Check with your state poultry specialist, veterinarian, or veteri- 
nary products supplier regarding the latest regulations. Carefully follow the 
label directions of any drug you use. 


In the number of species involved and the damage they do to chickens, round- 
worms are die most significant parasiric worm. They belong to the phylum 
Nemathelminthes (nema means "thread" and helinins means "worm" in 

Internal Parasites: Worms 83 

Nematodes are less common in caged layers than in floor-reared birds. 
Direct-cycle nematodes and those requiring an indoor-living intermediate 
host (such as cockr oaches or beetles) are more of a problem in penned birds; 

tediate host (such 


Not all nematode eggs are infective when they are expelled from a chicken. 
Some require development or "embryonation" to become infective. Some 
eggs embryonate in as little as 3 days, others require 30 days or more. 

In order to embryonate, nematode eggs must encounter just the right con- 
ditions of temperature and humidity. In less than favorable conditions, 
embryonation may take longer or may not occur at all. In general, eggs 
embryonate more quickly under fairly warm, humid conditions. Minimizing 
moisture inhibits embryonation and slows the buildup of parasite loads. 

Large Roundworm 

The large roundworm (Ascaridiagalli) is one of the most common poultry 
parasites. Roundworm or ascarid infestation is called "ascaridiasis." The large 
roundworm is approximately the same thickness as pencil lead and grows as 
long as 4'/2 inches (9 cm) — big enough to be seen without a magnifying glass. 

Adult large roundworms roam a chicken's small intestine. Occasionally 
one will migrate from the intestine up the cloaca and get trapped inside a 
newly forming egg — a decidedly unappetizing occurrence. Such a round- 
worm can easily be detected during candling. 

One female roundworm lays up to 5,000 eggs, which take 10 days or more 
to embryonate. Embryonated eggs survive in the soil for a year or longer. 
Roundworms are spread by direct cycle — embryonated eggs are picked up by 
a chicken from droppings, soil, feed, and water. 

Birds that are over 3 months old are more resistant to ascaridiasis than 
younger birds. Heavier breeds such as Rhode Island Red and Plymouth Rock 
are more resistant than lighter breeds such as Leghorn and Minorca. Chickens 
diat eat primarily animal protein are more resistant than chickens that eat pri- 
marily plant protein. 

Signs of ascaridiasis are pale head, droopiness, weight loss or slow growth, 
emaciation, and diarrhea. In a severe infestation, the intestines become 
plugged with worms, causing death. Even a somewhat mild infestation may be 
devastating when combined with some other disease, particularly coccidiosis 
or infectious bronchitis. In addition, ascarids have been implicated in the 

84 Tiu: Cnrnm Bmim ! Handbook 

Of the drugs approved for ascarids in chickens, only piperazine is readily 
available to owners of small-scale flocks, although levamisole is often used for 
backyard flocks, particularly exhibition birds. Piperazine affects only adult 
roundworms. When an embryonated egg hatches in a chicken's intestine, 
within 7 days the new young worm attaches itself to the bird's intestinal lining. 
Although Ibis immature form does more damage than an adult roundworm, 

Whenever you worm your flock, repeat the worming in 7 to 10 days, giving 
young worms time to release their hold on the intestinal lining. 

Capillary Worm 

Six species of Capillaria or capillarids invade chickens, causing "capil- 
lariasis." Capillarids are white, hairlike or threadlike worms. Most are too small 
to be seen with die naked eye, but may be seen witii die aid of a magnifying 
glass. They usually lodge in a chicken's crop, ceca, and/or intesdnes. In a seri- 
ous infestation, worms may move into the bird's throat or mouth. 

Most capillarids have an indirect cycle, with earthworms as the intermedi- 
ate host. Some have a direct cycle. One species (C. Contortaj is both direct and 
indirect. Capillarid eggs are small and difficult to idendfy during fecal exami- 
nation (described later in this chapter). 

Symptoms of capillariasis are pale head, poor appetite, droopiness, weak- 
ness, emaciation, and sometimes diarrhea. Chickens may sit around wit h their 
heads drawn in. Postmortem examination (described in chapter 10) may re- 
veal adult worms in a thickened and inflamed crop. 

Capillariasis is most likely to occur in flocks kept on built-up litter. No ap- 
proved treatment is readily available to small-flock owners; levamisole is often used. 

Crop Worm 

Easily confused with capillary worm, the threadlike crop worm 
(Gonglyonema ighwicola) invades the crop and sometimes the esophagus and 
proventriculus (stomach). Its indirect cycle involves beedes and cockroaches. 

Unless diey get out of hand, crop worms do little damage. Signs of a seri- 
ous infection are droopiness, weakness, lack of activity, reduced appetite, and 
thickening of the crop wall. Crop worms can be controlled by controlling 
beetles and cockroaches. 

Cecal Worm 

The cecal worm (Heterakis gallinanim) is die most common parasitic wonn in 
North American chickens. As its name implies, it invades a bird's ceca. Otiier 

Internal Parasites: Worms 85 

than carrying blackhead, to which most chickens are immune, the cecal worm 
does not seriously affect a bird's health. Leghorns are more susceptible to this 
parasite than heavier breeds such as Rhode Island Red and Wyandotte. 

Cecal worms are slender, white, and about V*-inch long, making them easy 
to see. Their cycle is direct. Eggs embryonate in 2 weeks (longer in cool 
weather) and survive for long periods under a wide range of environmental 
conditions. Phenothiazine is the approved method of treatment, although 
many backyard flocks are treated wiih levamisole. 

Strong\'lokles avium is another parasite that invades the ceca, primarily in 
chickens raised in Puerto Rico. This worm is unusual for two reasons. First, 
rather than hatching in an animal host, it's eggs hatch in soil, where mature 
worms live and grow. Second, only the female worm parasitizes chickens. In- 
festation can be deadly to young birds, but may cause no symptoms in adult 
birds. No approved treatment is available for small flocks; levamisole is often used- 
Stomach Worm 

The stomach worm (Telrameres americana) invades a chicken's proven- 
triculus, causing anemia, emaciation, diarrhea, and in a severe infestation, 
death. This worm is such a bright red color that you can sometimes see it 
through the wall of an unopened stomach during postmortem examination 
(see chapter 10). On close inspection, you will find worms of two shapes: the 
elongated ones are male, the roundish ones are female. 

T. americana has an indirect lifecycle involving cockroaches and grass- 
hoppers. Its near relative T. fissispina, which is identical but considerably 
smaller, is carried by the same intermediate hosts and also by earthworms and 
sand hoppers. Control of the stomach worm involves controlling its inter- 
mediate hosts. 

Eye Worm 

Eye worm (Oxyspirura mansoni) is prevalent in the southern United 
Stales, Hawaii, the Philippines, and other tropical and subtropical areas. It is a 
small white worm that lodges in die corner of a chicken's eye. The eye becomes 
swollen, inflamed, and watery , impairing the chicken 's vision. The eyelids may 
stick together and the eye may turn cloudy and eventually be destroyed. 
Meantime, the chicken scratches the eye, trying to relieve irritation. 

Eye worms have an indirect cycle. Worm eggs deposited in the eye pass 
into die tear duct, are swallowed by the chicken and expelled in droppings, 
and are eaten by the Surinam cockroach (Pycnoscelus surinamensis). When a 
chicken eats an infective cockroach, worm larvae migrate up the esophagus to 

86 The Chicken Health Handbook 

Chart 5-1 

Roundworms (Nematodes) 

Common Name 


Scientific Name 



capillary worm (capillarid) 
CapiUaria anatis 

capillary worm (capillarid) 

C. annulata 
capillary worm (capillarid) 

C. contorla 

capillary worm (capillarid) 

C. obsignata 
capillary worm, threadworm (capillarid) 

C. bursata 
capillary worm, threadworm (capillarid) 

C. caudinflata 
cecal worm 

Heterakis gallinantm 

cecal worm 

Strongyloides avium 

cecal worm 

Subulura brumpti 
cecal worm 

S. strongylina 

crop worm 

Congylonema ingluvicola 

eye worm, Manson's eye worm 
Oxyspirura mansoni 

gapeworm, forked worm, red worm 
Syngamns trachea 

gizzard worm 

Cheilospirura hamulosa 
roundworm, common 

Trichostrongulus tenuis 

roundworm, large (ascarid) 
Ascaridia galli 

while, threadlike, 0.3-1" 
(8-28mm) long 

white, threadlike, 0.04-2.4" 
(1-60 mm) long 
white, threadlike, 0.3-2.4" 
(8-60 mm) long 

white, threadlike, 0.3-0.7" 
(7-18 mm) long 
white, threadlike, 0.4-1.4" 
(1 1-35 mm) long 
white, threadlike, 0.3-1" 
(9-25 mm) long 
yellowish-white, thin, 0.3-0.6" 
(7-15 mm) long 

white, free-living, tiny, 0.08" 
(2.2 mm) long 

white, 0.3-O.6" (7-14 mm) long 

white, 0.2-0.7" (4.5-18 mm) 

white, threadlike, 0.7-2.2" 
(17-55 mm) long 

white, slender, 0.3-0.8" 
(8-20 mm) long 

red, Y-shaped, 0.2-0.8" 
(5-20 mm) long 

reddish, 0.4-1" (9-24 mm) long 

white, slender, 0.2-0.4" 
(5.5-1 1 mm) long 

yellowish white, thick, 2-4.5" 
(50-1 15mm) long 


none or 



beetle, earwig, 








none or 


slug, snail 




stomach worm 

Tetrameres americana 
stomach worm 


stomach worm, spiral 
Dispbarynx nasitta 

bright red, male: long, 0.2" (5 
mm) female: round, 0.16" (4mm) 
similar to T. americana but 
smaller 0.06-0. 16" 
(1.5-4.1 mm) long 

white, coiled, 0.3-0.4" 
(7-10 mm) long 








'Use not approved — consult a veterinarian. 

Internal Parasites: Worms 87 






sometimes small 
intestine, cloaca 
crop, esophagus 

crop, esophagus, 



small intestine, 

small intestine 
small intestine 


sometimes small 




crop, sometimes 

bronchi, lungs 



sometimes small 
small intestine, 
esophagus, crop, 





weakness, emaciation, 
possible diarrhea, death 

emaciation, death 

weakness, emaciation, reluctance to 
move, possible diarrhea, death 

huddling away from flock, weakness, 
emaciation, possible diarrhea, death 
pale head, inactivity, reduced appetite, 
slow growth, possible diarrhea, death 
pale head, inactivity, reduced appetite, 
slow growth, possible diarrhea, death 
weakness, weight loss (carries 

none or pasty cecal discharge, turning 
thin and bloodv (found in Puerto Rico) 

none, (found in Puerto Rico and S. 
America, not N. America) 

droopiness, weakness, inactivity, 
reduced appetite, slow growth, 
thickened crop wall 
scratching of eyes; watery, inflamed, 
swollen eyes; eyelids stuck together 

gasping, coughing, eyes closed, head 
drawn in, yawning, head shaking, 

usually none 

primarily in young birds; weight loss, 
anemia, deaths peak in spring and fall 

pale head, inactivity, reduced appetite, 
slow growth, diarrhea, deadi 

diarrhea, anemia, emaciation, death 
diarrhea, anemia, emaciation, death 

heavily infested birds may die 












^^^^^^^^^^ ♦ 











severe in 


young birds 




low) i^iic/^Iq* 






ivermectin (3 

drops in eye 

twice daily) 



moderate in 

adult birds 




intermed. host 











intermed. host 









88 Tut; Chicken Health Handbook 

by eye worm, and may help spread it to chicken flocks. Eye worm is controlled 
by controlling cockroaches around the hen house. 

Veterinary treatment, usually reserved for valuable birds, involves apply- 
ing a local anesthetic to the eye, carefully lifting the third eyelid, applying 1 or 2 
drops of 5 percent cresol solution, and immediately flushing out the eye with 
clean water. If the eye is treated in the early stage of infection, it should clear up 
in 2 or 3 days. 

An alternative (unapproved) treatment involves putting 3 drops of 
ivermectin into the chicken's eye, twice a day, until the eye worms are gone. 


The gapeworm (Syngamm trachea) buries its head in the lining of a bird's 
windpipe or other part of the respiratory system, causing "the gapes" or 
"gapes." Gapeworms get their name from the habit an infected bird has of 
continually yawning or gasping for air. These worms, which are big enough to 
be seen without magnification, are also called "red worms" or "forked worms" 
- each blood-red female has a somewhat paler male permanently attached, 

Gapeworms can cause considerable losses in free-ranged flocks, particu- 
larly those associated with adult turkeys. This parasite is especially serious in 

An infected chicken coughs up worm eggs, swallows them, and expels 
them in droppings. The cycle is ei ther direct or indirect, involving earthworms, 
slugs, and snails. Eggs take up to 2 weeks to embryonate and may survive in soil 
for as long as 4 x h years. 

Symptoms of gapes are yawning, gamting, gasping, sneezing, coughing 
(sometimes coughing up a detached worm), choking, loss of energy, loss of 
appetite, weakness, emaciation, closed eyes, head shaking, frequent throwing 
of head forward with mouth open to gasp for air, and convulsive shaking of the 
head (to dislodge worms from the windpipe). Gapeworms multiply rapidly, 
eventually suffocating the bird. 

Thorny-Headed Worm 

The thorny-headed worm (Acanthocephalans) is more common in Asia 
than in North America. It invades a chicken's intestine, causing anemia and 
weakness. Like the nematode, it is cylindrical in shape. It can be identified by 
its tubular sucking appendage, or proboscis, sporting curved hooks or spines. 

These worms have an indirect life cycle. Intermediate hosts include 
snakes, lizards, and a variety of arthropods (spiders, mites, ticks, cendpedes, 
and insects). Mebendezole, although not approved, is used as a treatment. 

INTERNAL Parasites: Worms 89 


Flatworms belong to the phylum Platyhelminthes [platys meaning "flat" and 
helmins meaning "worm" in Greek). Flatworms come in two versions, ribbon- 
shaped tapeworms (cestodes) and leaf-shaped flukes (trematodes). 


An estimated 50 percent of all chickens in small flocks are infested with 
tapeworms. Like roundworms, tapeworms come in many species. The eight 
species thai invade chickens range in size from microscopic to 13 Vz inches (34 
cm) long. Infestation is called "cestodiasis." 

Most tapeworms are host specific — those infecting chickens invade only 
chickens and their close relatives. All tapeworms lodge in the intestinal tract, 
attaching their heads to the intestine wall with four pairs of suckers. Each spe- 
cies prefers a different portion of the intestine. 

During postmortem examination (see chapter 10), most tapeworms can 
easily be seen without benefit of magnification. The exception is the micro- 
scopic tapeworm Davainea proglottina. To see it, open a portion of the 
duodenal loop and place it in water. The loose ends of the tapeworms will float 
away from the intestinal tissue. 

Ironically, this smallest species is also the most deadly. As many as 3,000 
have been found in one bird. Symptoms include dull feathers, slow move- 
ment, emaciation, breathing difficulty, paralysis, and death. General 
symptoms of cestodiasis are weight loss and decreased laying. Leghorns tend 
to be more resistant than Plymouth Rocks. 

All tapeworms require an intermediate host; an ant, beetle, earthworm, 
housefly, slug, snail, or termite. Caged birds are likely to be infected by worms 
whose cycle involves flies. Litter-raised flocks are likely to be infected by 
worms whose cycle involves beetles. Free-ranged chickens are likely to be in- 
fected by worms whose cycle involves ants, earthworms, slugs, or snails. 

A tapeworm's body is made up of individual segments, one or more of 
which break away each day. A chicken starts shedding segments within 2 to 3 
weeks after eating an infective intermediate host. In a severe infestation, you 
may see segments in droppings or clinging to the area around the vent, looking 
like bits of white rice. Each segment contains hundreds of eggs — in its life- 
time, each tapeworm releases millions of eggs, ensuring that some survive. 

Tapeworm Control 

To control tapeworm, you must control the intermediate host. Since 
symptoms are similar for most tapeworm species, it's important to know 
which species you're dealing with so you'll know which intermediate host(s) 

90 The Chicken Health Handbook 

you are looking for. 

Exterminating beetles is particularly troublesome, since not all beetles 
found in and around chicken coops are harmful. In fact some are beneficial. 
To complicate the matter, tapeworms are carried by numerous species includ- 
ing darkling, dung, and ground beeties. Ask your county Extension agent or 
state poultry specialist for information on problem beetles and dieir control in 
your area. 

Although no drug is currentiy approved to combat tapeworm, a veterinar- 
ian can provide a suitable medication. Luckily, tapeworm is not a major 
poultry disaster. 


Trematodes or flukes belong to the same phylum (Platyhelminthes) and 
class (Cestoda) as tapeworms, but are in the order Galliformes. Their only simi- 
larity to tapeworms is that both are flat. The fluke is leaf-shaped rather than 

Chart 5-2 

Common Name 
Scientific Name 

Tapeworms (Cestodes) 


Intermediate Host 

large chicken tapeworm 

large chicken tapeworm 
Raillietina cesticillus 

large chicken tapeworm 
R. cncliinobolhrida 

large chicken tapeworm 
R. tetragona 

microscopic tapeworm 
Davainea proglottina 

short tapeworm 
Amoebotaenia cuneaia 

short tapeworm 

threadlike tapewomi 

H. caricca 

very white, flat, segmented, 
up to 9" (23 cm) long 

white, flat, segmented, up to 
6" (15 cm.) long 

white, flat, wide, segmented, 
up to 13.5" (34 cm) 

while, flat, wide, segmented, 
up to 10" (25 cm) long 

white, flat, segmented, less 
than .16" (4 mm) long 

whitish, flat, segmented, less 
than 0.16" (4 mm) long 

white, flat, segmented, up to 
0.8" (2 cm) long 

while, flat, segmented, 
slender, threadlike, up to 0.5" 
(12 mm) long 

beetle (several 
species), housefly 

histerid and darkling 



slug, snail 

dung beetle 
(S. carabeidae) 

dung and ground 
beetle, termite 

Internal Parasites: Worms 91 

ribbon-shaped. It is not as host specific as the tapeworm, so it may be intro- 
duced to an area by wild birds. 

Flukes are rarely serious except where poor living conditions allow a mas- 
sive infestation. The four species that infect chickens each prefer a different 
part of the body — eye, skin, oviduct, or lower excretory system — where they 
attach themselves with two suckers. 

The oviduct fluke causes a hen's oviduct to swell and sometimes rupture, 
resulting in the hen's deadi. Early symptoms of infection include droopiness, 
weight loss, chalky white droppings, reduced egg production, soft-shelled 
eggs, and finding a fluke encased in an egg. 

The skin fluke forms Ve- to Vi-inch (4-6 mm) cysts under the skin, usually 
near the vent. The cysts, each containing two flukes, ooze and attract flies, 
leading to a possibly fatal bacterial infection. Meantime, the chicken suffers 
from depressed appetite and has difficulty walking. Treatment requires surgi- 
cally removing die flukes. 

Flukes have complicated life cycles that involve two intermediate hosts. 

Part of Intestine 

Affected Symptoms Severity Treatment 

small intestine 

duodenal loop, 
small intesiine 

large intestine 
large intestine 
duodenal loop 
duodenal loop 
duodenal loop 

duodenal loop 




weight loss, sevefe 


laying severe 





approved for 
| — poultry; see 


92 The Chicken Health Handbook 

Breaking the cycle is therefore easier than breaking the cycles of roundworms 
or tapeworms. The scenario goes something like this: Fluke eggs pass out of an 
infected chicken, are picked up by and develop within a snail, are released by 
the snail in water, swim around until they're eaten by a dragonfly or mayfly, 
and infect a chicken that eats the dragonfly or mayfly. The easiest way to con- 
trol flukes is to keep chickens away from ponds, lakes, or swamps where 
dragonflies and mayflies abound. 


Body Part Affected 

Collyriclum faba skin 

Philopluhalmus gmlli eye 

Prosthogonimus macrorchis (P. ovahis) oviduct 

Tanaisia bragai lower excretory system 

Fecal Test 

Some internal parasites can be identified by signs that appear in tine infected 
bird's droppings. Checking droppings may therefore help you identify the 
parasite so you can determine appropriate management changes and/or 
treatment, and so you can avoid the unnecessary use of wormers due to guess- 
work. You may discover that your chickens are not seriously infected with 
parasites, giving you reason to look for some other cause if your flock is experi- 
encing problems. 

Checking droppings, or more properly called "conducting a fecal exami- 
nation," can be done by any veterinarian, usually for only a few dollars. There 
are, however, good reasons to learn how to do your own testing. A 
veterinarian's office might not be handily nearby, discouraging you from test- 
ing as often as you would like. Mailing samples doesn't solve the problem, 
since samples dry out and parasite eggs may hatch or disintegrate. Even when 
you do your own testing, if you find something that looks serious, you might 
then wish to have your findings confirmed by a veterinarian before making 
drastic management changes or initiating drug treatment. 

Home Test 

Conducting your own fecal examinations is not difficult. To get an idea 
what's involved, take a fecal sample to your veterinarian and ask to have a look 

Internal Parasites: Worms 93 

when the sample is placed under a microscope. The vet will help you identify 
anything that is found. Once you know what you're looking for, you will have 
an easier time identifying signs of parasites on your own. 

The parasites in a bird's digestive tract release eggs, larvae, cysts, seg- 
ments, and sometimes mature adults in a bird's droppings. Parasites in die 
respiratory system may be coughed up and swallowed to appear in the bird's 
feces. Even external parasites, especially miles, are sometimes pecked by a 
bird and turn up in its droppings. 

You can collect droppings from the ground or floor, if you're certain 
they're fresh. Otherwise, obtain a sample directiy from a bird: place your hand 
inside a plastic bag, persuade the bird to do its duty, and wrap the sample by 
turning the bag inside out over the sample. If you're checking the whole flock 
rather than individual birds (for example, new birds you're just bringing in), 
collect about a dozen samples and mix diem together. 

Examine the sample for clearly visible signs of dead worms or tapeworm 
segments. Whether or not you find anything, die next step is to examine the 
sample under a microscope. The most likely thing you'll see is parasite eggs. 
Some eggs are unique and easy to recognize. Others are quite similar within a 
group, making it difficult to tell one species from another. Either way, you'll 
need a pictorial guide such as Veterinary Clinical Parasitology (listed in the ap- 

Be aware that some things a bird eats that turn up in its droppings may 
resemble parasites. Such "pseudo-parasites" include mold spores, pollen 
grains, grain mites, and corn smut spores. The latter can easily be mistaken for 
tapeworm eggs. 

Examination Kit 

To conduct a fecal examination, you'll need a microscope, preferably one 
that magnifies from 100 times to 400 times. A good microscope can cost hun- 
dreds of dollars, unless you find one at a flea market or garage sale. An 
inexpensive microscope, designed to introduce children to science, is suffi- 
cient for most home purposes. As an alternative to purchasing a microscope, 
you might persuade a local high school or college biology instructor to let you 
bring in your samples for examination. 

Most of die other things you'll need are ordinary items found around the 
average house. If your microscope is an inexpensive one, you'll need a light for 
it — which can be as simple as a well-directed strong flashlight beam or a 
hand-held egg candler. 

The most difficult to find items, though not expensive, are microscope 
slides and test tubes. Look for them at medical supply oudets or ask your drug- 
gist to get them for you. If you purchase a student microscope, it may come 

94 The Chicken Health Handbook 

lually you'll need replacemenl covers. 

Unless you plan to test more than one sample at a time, you'll need only 
one test tube (it doesn't hurt to have at least one spare). To hold the test tube in 
an upright position, make a stand by drilling a hole in a block of wood or 
styrofoam so the tube fits snugly. 

To speed up the separation of eggs from other fecal matter, professionals 
use a centrifuge fa machine that spins to separate particles of varying densi- 
ties). At home, your options are to examine a simple smear or use the flotation 

Fecal Examination Kit 




100X to 400X magnification 

Specimen cups 

3 ounce (90 ml) paper cups 

Wooden sticks 

tongue depressors or Popsicle sticks 


small tea strainer 

15 cc test tube 

'/i"x4" (12 mm x 10 cm) long 

Test tube holder 

wooden or styrofoam block 

Flotation solution 

sugar and tap water 

Medicine dropper 

eye dropper 

Microslides with cover slips 

standard 3" xl" (75x25 mm) 



Veterinary Clinical Parasitology 

Identification guide 

Simple Smear Method 

The simple smear method is not very accurate, but it's better than nothing, 
and it gives you something to do while you're waiting for eggs to separate for 
die flotation method. 

Begin by placing your microscope on a piece of a magazine or newspaper 
in such a way that you can look through the microscope to read the print. Put a 
slide into the microscope and use an eye dropper to place a drop of water in die 
center of the slide. 

With a toothpick, pick up a Va-inch (3 mm) blob of droppings and stir it 
into the water droplet until the water turns cloudy. You should still be able to 
see the printed page through die moistened sample. If necessary, use tweezers 
to pick out large pieces of debris. Place a cover slide over the sample and sys- 
tematically examine the sample through die microscope. 

Internal Parasites: Worms 95 

Flotation Method 

The aim of the flotation method is to separate out eggs or larvae so you can 
more readily see them. When you combine the feces sample with a flotation 
solution, eggs will float and heavier fecal matter will sink. 

To make the flotation solution, combine 2Va cups of sugar (454 g) with IV2 
cups (355 ml) of tap water in a small saucepan. Stirring, heat the mixture until 
it turns clear. Pour the solution into a clean, labeled jar and keep it in the refrig- 
erator until you need it. 

When you're ready for the test, use a wooden stick to transfer a '/2-inch (2- 
3 g) blob of fresh fecal matter into a paper cup (more is not better here — too 
much fecal matter will make your sample too thick to strain). Measure out one 
and a half test tubes of flotation solution into the cup. With the wooden stick, 
mix the sample and solution thoroughly, taking care not to stir up air bubbles. 
Pour the liquid through a strainer into a second paper cup. Stir and press out as 
much liquid as you can. 

Important sanitation measure: Before proceeding, seal the first cup con- 
taining solid fecal matter in a plastic bag for disposal and clean the strainer by 
pouring boiling water through it. 

Place the test tube in a holder and pour the liquid from the second cup into 
the test tube. If necessary, use an eye dropper to top off the test tube with fresh 
flotation solution until the liquid rises above the rim, but does not run over the 
edge. Using tweezers, place the slide cover slip on top, taking care not to leave 
an air bubble beneath the slip or jostle die tube so it overflows. 

Leave the cover slip on the test tube for 3 to 6 hours, during which parasite 

Fecal samples can be examined for 
nematodes and oocysts using a low- 
powered microscope. 

Flotation solution rising above test 
tube rim. 

96 The Chicken Health Handbook 

eggs will float to the top. \ good thickness of material should stick to the bot- 
tom of the slip. 

With tweezers, carefully lift the slip straight upward and put it in the center 
of a microscope slide, taking care not to create air bubbles. Avoid squeezing 
the slide and cover together, or you might mash the evidence. 

Place the slide in the microscope and systematically examine it under 400X 
magnification. (For protozoan oocysts, described in chapter 6, set the micro- 
scope at 1 00X). Compare anything you find with photos in your identification 

Finding a few parasite eggs is normal and no cause for alarm. A count of 

tion, which translates into about 1,000 eggs per Mi-inch blob of droppings. A 
count of more than 1,000 EPG (or about 1,200 eggs per Vfe-inch blob) means 
prompt treatment is necessary. Of course, you would need a centrifuge to spin 
this many eggs from any sample, but you can see that there's a vast difference 
between finding a few eggs on your slide and even a "moderate" infestation. 

When you're done with your fecal test, clean out the test tube with an old 
toothbrush labeled for the purpose. Rinse all your materials with boiling water 
and set them on a paper towel to dry before putting them away. Store your 
microscope away from moisture and dust. 

Internal Parasites: Protozoa 

PROTOZOA ARE SINGLE-CELLED CREATURES that look round when viewed 
through a microscope. They are the simplest members of the animal kingdom 
and also die smallest, ranging in size from 1 to 50 microns (0.00004 inch or 
'/i,ooo mm) — too small to see widi the naked eye. Many protozoa are harmless. 
Others are parasites, causing serious diseases. 

Two phyla of protozoa affect chickens: Apicomplexa and Sarcomasti- 
gophora. Included in them are several genera that cause a variety of diseases in 

Chart 6-1 

Protozoan Diseases 







cloaca, cloacal bursa, 


lungs, air sacs, eye lids 



ceca or intestines 




ceca and liver 

very rare 



blood, liver, lung, spleen, 





blood, liver, lung, spleen. 





central nervous system 

very rare 



mouth and throat 



98 The Chicken Health Handbook 

chickens, some of them quite serious. Luckily, the worst protozoan parasites 
are rare or are not found in North America. 


Coccidiosis is die most common and most widely known protozoal disease of 
poultry. It is caused by several different species of protozoa known as coccidia, 
most of which are in the Eimeria genera. Cocci is the most likely cause of death 
in growing birds, usually striking chicks 3 to 6 weeks of age. The worst cases are 
likely to occur at 4 lo 5 weeks. 

Coccidia are found wherever there are chickens. Even in the healthiest 
flock, coccidia are present in the intestines of most birds over 3 weeks old. 
Many species cause no disease or only mild disease, in which case die chickens 
are said to have "coccidiasis." 

Gradual exposure (or surviving an infection) allows a chicken to become 
immune to the disease-causing coccidia in its environment, so by maturity 
most chickens are immune. Chickens wiUi Marek's disease are an exception, 
since diey don't always develop the same immunity to coccidiosis as healthy 
chickens do. Immune chickens won't get coccidiosis, unless their resistance is 
reduced by some other disease or they're exposed to a new species of coccidia. 

A devastating outbreak may occur when a large number of growing or 
mature birds are brought together from different sources, since diey may not 
all have been exposed to (and therefore developed immunity to) the same coc- 
cidia species. Outbreaks also occur where sanitation is poor and/or birds are 
stressed due to overcrowding, an abrupt change in radons, being transported, 
or some drastic change in the weather. 

Life Cycle 

Coccidia have short, complex, direct life cycles. A chicken eats an infective 
egg, or oocyst, containing eight coccidia in a form known as a "sporozoite." 
The oocyst is crushed in die bird's gizzard, releasing the eight sporozoites, 
which lodge in the bird's intestine wall and begin to reproduce. Within 4 to 6 
days, the reproductive cycle goes through two or more generations (the lengdi 
of time and number of generations vary widi coccidia species), at the end of 

which millions of oocysts are released in 
the chicken's droppings. 

The life cycle of protozoa resulting 
from the first oocyst is now over, making 
coccidiosis a self-limiting disease with 
potentially inconsequential results. 

Oocysts: E. renella (left), E. acenntlina 

Internal Parasites: Prota/.oa 99 

on the number of oocysts it eats — in a highly contaminated environment, one 
chicken may eat between one thousand and one million infective oocysts. 

To become infective, the oocysts must develop or "sporulate" (the proto- 
zoal equivalent of embryonation in nematodes). For most species of coccidia, 
sporulation takes 18 hours or less. When a chicken eats a sporulated oocyst, 
the cycle begins again. 

damp litter, feed, and drinking water. As birds either die or recover and the 
infection plays out, the number of shed oocysts decreases. Oocysts are sensi- 
tive to ammonia, molds, and bacteria, so they do not survive long in litter. 
Continuing litter contamination requires constant shedding by infected birds. 

In soil, given the right moisture and temperature, oocysts can survive for 
several weeks (up to 18 months under ideal conditions). They can't survive 
long in dry soil, and they don't survive at temperatures below freezing or above 
130°F (55°C). The danger of an outbreak is therefore greatest during warm, 
humid weather. Chicks hatched in late winter or early spring therefore tend to 
be healthier than chicks hatched during the wanner, more humid summer 

The first outbreak of coccidiosis in a new chicken coop is usually the worst, 
a phenomenon known as "new-house coccidiosis syndrome." The reason is 
that the first birds raised on new ground have little exposure to infective oo- 
cysts. When they eventually become exposed, they have little or no immunity 
and die outbreak is particularly serious. 

Oocysts are spread on the feet of wild birds (even though the wild birds 
themselves don't become infected), on the bodies of insects and other ani- 
mals, on people's shoes, on the tires of feed delivery trucks, and on used 
equipment that hasn't been thoroughly cleaned. 

Coccidia irritate the intestinal lining, interfering with the absorption of nu- 
trients. Outbreaks range from so mild you don't notice your chickens are sick 
to so severe they die. In mature birds, the chief sign is slow or no egg produc- 
tion. Breeds with yellow shanks and skin may turn pale due to their reduced 

a source of infection for younger birds. 

In young birds, symptoms include slow growth, a change in the droppings 
(runny, off-color, sometimes tinged with blood), and dehydration due to diar- 
rhea. The disease may come on slowly, or bloody diarrhea and deaths may 
come on fast. The weakened chickens become more susceptible to odier para- 
sites and diseases. Intestinal tissue damage causes the birds to be especially 
susceptible to bacterial infections such as salmonellosis or necrotic enteritis. 

100 The Chicken Health Handbook 

Chart 6-2 

Coccidia Affecting Chickens 

Species Invades 

Eimeria acervulimf* duodenal loop 

i> Rbmnetti" 

lower small intestine and ceca 

& E. hagani 

duodenal loop 

S maxima" 

middle portion of small intestine 

' Rmitis 

lower small intestine 

E. mivatv 

entire intestine (starts in upper 
portion and works its way down) 

8 E. iiecatrix** 

middle portion of small intestine 

/:'. praecox 

duodenal loop 

:> Etenella** 


*See Chapter 10. **Main causes of clinical outbreaks. 

Internal Parasites: Protazoa 101 


Postmortem Findings* 


(usually in chicks 3 to 6 weeks old) 
slow growth, pale skin 

roughened wall of duodenal loop 
with gray or white round or 
striped patches (under magni- 
fication), sometimes overlapping 


slow growth, bloody droppings, 
up to 30% mortality; survivors 
do not grow well 

peeling away of intestine large, 
lining oval 

watery diarrhea 

tiny bloody spots along 
duodenal loop wall 

oval to 

(usually chicks 3-6 weeks old) 
slow growth, pale skin, rough 
feathers, yellow, gray, or brown 
diarrhea, loss of appetite, weight 
loss, high mortality 

reddened, distended, large, 
thickened small intestine yellow- 
Filled with grayish, pinkish, ish, oval 
or orange brown mucus 

slow growth, weight loss, pale skin none significant 


slow growth 

thickened intestine wall 
with patches similar to 
E aceri'itlinabui rounder 


(usually in birds 8 to 18 weeks old) 
conies on fast; weight loss, watery, 
bloody diarrhea, up to 25% mortality 

portions of intestine may be 
twice the normal size, filled 
with blackish blood clots, lining 
thickened, mottled with white 
spots or bloody (red or black) dots 


slow growth, pale skin, watery 
diarrhea, dehydration 

intestine filled with watery roundish 
fluid, small red dots along to oval 


(usually in chicks 3 to 6 weeks old) 
comes on fast; slow growth, weight 
loss, bloody diarrhea, severe anemia 
high mortality (bacterial infection); 
survivors do not grow well 

ceca filled with clotted blood 
and dead tissue that turns 
blackish, hardens and is 
eventually expelled in droppings 


102 Ti ie Chicken Health Handbook 

Coccidiosis is worse in a flock that's combating another disease; cocci often 
follows an outbreak of infectious bursal disease. 

In severe cases, destruction of the intestinal lining causes hemorrhaging 
and death. In any case, internal damage is often done before you notice the 
first symptoms. Seriously damaged birds never become as productive as unaf- 
fected birds. It's therefore best to manage your flock with cocci in mind, rather 
than to wait and treat the disease after it occurs. 

If you do suspect coccidiosis, a fecal test (described in chapter 5) will tell 
you whether or not your birds are shedding oocysts and will help you pinpoint 
the species. Several tests may be required to identify the species, since an in- 
fected chicken does not shed oocysts at a steady rate. In diagnosing the cause 
of an outbreak, you can pretty safely eliminate any species that previously in- 
fected your flock. If you conduct a postmortem examination (see chapter 10), 
do so immediately after death — within an hour, changes occur that make 
diagnosis more difficult. 

Coccidia Species 

Eimeria protozoa come in many species that infect nearly every kind of 
livestock, but each is highly species specific — the coccidia that invade chick- 
ens do not affect other kinds of livestock, and vice versa. Even different kinds 
of birds are infected by different species of coccidia. 

In chickens, coccidiosis is caused by nine species of Eimeria protozoa, 
some more serious than others. One bird may be infected with more than one 
species at a time. Each species is identifiable by a number of traits including 
the portion of a chicken's intestinal tract it prefers, the appearance of its oo- 
cysts (size, shape, and color), and the symptoms it produces. 

E. acervulina is the most common cause of coccidiosis in North America. 
E. tenella and E. necatrixare the most serious, coming on rapidly and resulting 
in high death rates. £. tenella, a form of cecal coccidiosis, generally infects 
chicks 3 to 6 weeks of age. E necatrix, a form of intestinal cocci, takes longer to 

Cocci Control 

Measures for controlling coccidiosis involve, in order of preference: 

• good management 

• the use of drugs 

• vaccination 

Good management includes providing adequate dry litter, clean drinking 
water, and proper nutrition. All ground-fed chickens are exposed to infective 

Internal Parasites: Pkotazoa 103 

oocysts throughout their lives. A 
well-managed flock quickly de- 
velops resistance. The sooner 
that happens, the healthier the 
chickens will be. 

Coccidiosis is generally less 
of a problem in free- ranged 
flocks, being more serious when 
chickens are concentrated in a 
small area. Chicks raised on wire 
and moved to litter when they're 
partially grown become seriously 
infected, since they have not had a chance to develop resistance through 
gradual exposure. Resistance is not necessary for caged layers and cage- 
managed show stock, since they are unlikely to be exposed to coccidia (unless 
dieir drinking water becomes contaminated). 

Vaccination against coccidiosis has limited success, although it is some- 
times used for breeder pullets. Vaccination is seldom used for broilers — die 
mild infection produced by the vaccine slows growth, making the option un- 
economical. Genetically engineered antigens, now on the horizon, may one 
day be used to immunize young chicks. 


A number of drugs are available to prevent or control coccidiosis. Which 
one you use, if any, and how you use it depends on whether your intent is to 
prevent infection, permit a mild infection thai allows resistance to develop, or 
treat an existing infection. The type of drug used and die dosage needed also 
vary with the species of coccidia involved — not all coccidiostats are effective 
against all species. 

Drugs designed for treatment require high dosage levels, yet an excessive 
dose can poison chickens. Since the toxic level of sulfamethazine is close to the 
level required for treatment, poisoning can occur at normal doses if high tem- 
perature causes an increase in treated water intake. Symptoms of poisoning 
are depression, paleness, and slow growth. At temperatures over 80°F (27°C), 
avoid poisoning by using only one-third the recommended dose. 

The use of some anticoccidials, particularly amprolium, causes vitamin 
deficiency. It's a good idea, therefore, to offer a vitamin supplement after you 
treat your flock. Do not use a vitamin supplement during treatment, because 
vitamin deprivation is one of the ways amprolium controls coccidia. Since 
coccidiosis increases a flock's susceptibility to bacterial infections, using an 
antibiotic along with the anticoccidial improves the rate of recovery. 

Chart 6-3 
Drugs Used to Treat Coccidiosis* 

Drug Application Time 

Amprolium water none 

Sulfadimethoxine water 5 days 

Sulfamethazine water 10 days 

Sulfaquinoxaline feed 10 days 

*For dosage and length of treatment, follow 
directions on label. 

104 The Chicken Health Handbook 

Some of the same drugs used to treat cocci, plus a few additional ones, are 
used in low dosages to prevent a serious outbreak in young birds while (at least 
theoretically) allowing them to develop immunity through gradual exposure. 
The use of drugs for this purpose, usually from the day of hatch to 16 weeks of 
age, does have drawbacks: 

• Although drugs used for treatment are equally effective in prevention 
— since they reduce the protozoa population by killing any coccidia a 
chicken eats — the chickens may not be exposed to adequate numbers 
of coccidia to become immune, so an outbreak may occur when the 
drug is withdrawn. 

• Drugs designed specifically for control (rather than treatment) suppos- 
edly reduce the degree of infection while allowing immunity to 
develop, but some only arrest the development of immunity, paving 
the way for an outbreak when they are withdrawn. Some are toxic at 
high levels and/or produce side effects. Any continuous low dose of 
medication in water or feed can lead to the development of drug- 
resistant strains of coccidia, requiring rotation of drugs used. 

• The medication has a withdrawal time of 30 days, so if you raise meat 
birds, you'll have to find a non-medicated brand of feed during diat 
last month. That being the case, why not seek out the alternative brand 
and use it right from the start? Feeds containing preventive medica- 
tion are designed for commercial producers who bring in as many as 
30,000 broilers at a time, and raise one batch right after another. In a 
small flock, the use of medication is a poor substitute for good 


Ciyptosporidiosis is the one form of coccidiosis that is not caused by Eimeria, 
but rather by the protozoa Cryptosporidium baileyi. Unlike the other forms of 
coccidiosis, cryptosporidiosis is not specific to chickens; it infects other birds 
and is possibly spread by wild species. Although C. baileyi does not invade 
mammals, it may be spread from flock to flock on the feet of animals and 

Like other coccidioses, cryptosporidiosis is spread by oocysts, but each 
contain four (rather than eight) sporozoites. The oocysts are considerably 
smaller than those of other coccidia, and detecting them requires special labo- 
ratory techniques. 

Like other coccidia oocysts, Cryptosporidia oocysts are sensitive to ammo- 
nia in litter. They are also somewhat sensitive to chlorine bleach as a 
disinfectant, and they cannot survive temperatures above 140° F (60°C). 

Internal Parasites: Protazoa 105 

Unlike FJmeria oocysts, those of Cryptosporidium are infective when they 
leave the host's body. Some may not leave at all, but remain and develop 
within the same host (called "autoinfection"). As few as 100 oocysts in one bird 
can quickly produce a serious infection. 

Although it has not been studied as thoroughly as other forms of 
coccidiosis, intestinal cryptosporidiosis is apparently quite common in chick- 
ens. It is usually mild, often producing no symptoms other than pale skin in 
yellow-skinned breeds. Once infected, birds become immune. 

Oocysts may be inhaled as well as ingested, causing respiratory infection 
that is less common though more severe than the intestinal form. Respiratory 
cryptosporidiosis is likeliest to affect birds in the 4- to 17-week age group. Sur- 
vivors begin recovering in 2 to 3 weeks. E. coli often produces a secondary 
infection, and an existing infection with E. coli or infectious bronchitis virus 
makes respiratory cryptosporidiosis worse. 

Cryptosporidia invade other parts of the body, including the eyelid and the 
cloacal bursa, from which they may travel up the urinary tract. No means of 
prevention or treatment is known. Chickens develop natural immunity when 
exposed to oocysts at low levels, leading to the possibility of a vaccine in 
the future. 


Infection with Histomonas meleagridis protozoan parasites is commonly 
known as "blackhead" because an infected bird's face tends to darken, al- 
though this is neither a sure sign of the disease nor necessarily characteristic of 
it. The disease — caused by round, microscopic histomonads — is serious in 
turkeys, but chickens are normally immune. 

Blackhead is more common in range-fed than housed or caged chickens, 
since die disease occurs when a chicken eats an earthworm carrying eggs of 
the cecal worm (Heterakis gailinaruin), which in turn are harboring histo- 
monads. The parasites lodge in the chicken's cecum, enter the bloodstream, 
and eventually migrate to the liver. 

Histomonads shed by infected chickens may reinfect the same chicken or 
infect another chicken that picks in droppings or eats a fly, sowbug, grasshop- 
per, or cricket carrying die parasite on its body. Once shed, histomonads 
cannot survive long in the environment unless they are protected by a cecal 
worm egg or an earthworm. 

Chicks 4 to 6 weeks old are the most susceptible to histomonad infection. 
Mild strains produce no symptoms; virulent strains may cause deaths in die 20 
to 30 percent range. Drugs approved in the United States are not particularly 
effective. Since survivors continue to shed histomonads. control requires con- 
trolling cecal worms (see "Cecal Worm," page 84), 

106 Tin: Chicken Health Handbook 


The protozoan Toxoplasma gondii causes toxoplasmosis in warm-blooded 
animals including chickens and humans. It is mainly a disease of the central 
nervous system, but may also affect the reproductive system, muscles, and in- 
ternal organs. 

This protozoa has a complex life cycle. A chicken may become infected in 
many different ways: picking in infected droppings of chickens, cats, or other 
animals; picking al an infected chicken, live or dead; eating earthworms har- 
boring toxoplasma oocysts. Toxoplasma may be spread from one area to 
another on the feet of rodents. 

Control involves keeping litter dry, controlling filth (lies, cockroaches, and 
rodents, and keeping the yard free of cats. No effective cure is known. 


The protozoan parasite Trichomonas occasionally infects chickens, causing a 
mouth and throat disease known as "canker." It is primarily a disease of pi- 
geons that may be spread to chickens through feed or water contaminated 
with discharge from an infected bird's mouth. Control involves keeping pi- 

not spread. 

Blood Parasites 

A chicken's blood may be invaded by a variety of protozoan parasites, most of 
which are not common in North America. 

Leucocytozoon are found near swampy areas and are spread by blackflies 
and biting midges, causing anemia and sometimes death due to hemorrhage. 

Plasmodium protozoa, transmitted by mosquitoes, cause malaria found 
in chickens in Africa, Asia, and South America, but so far (knock on wood) not 
in North America. 

Avoid these blood infections by controlling biting and bloodsucking in- 
sects such as blackflies, biting midges, mosquitoes, and flies. Do not allow 
weeds and trash to accumulate, as they provide breeding grounds for insects. 

Infectious Diseases 

THE INFECTIOUS DISEASES described in this chapter are caused by plant- 
like microscopic parasites — bacteria, viruses, and fungi. Some of these 
microflora are always present but cause disease only under certain circum- 
stances, such as when a chicken's resistance is low due to stress. Such 
microbes are called "opportunists." 

A few microbes produce disease wherever they occur. They are commonly 
known as "germs." but technically they are "pathogens," and are described as 
being "virulent" or "pathogenic." Variations in padiogenicity among strains 
cause the same disease to appear in different degrees of severity or even in 
different forms altogedier. 

The vast majority of microbes are either harmless or beneficial. Beneficial 
microflora may live on a chicken's skin or within its body, aiding digestion 
and/or enhancing the bird's immunity by fending off pathogenic microbes, a 
process known as "competitive exclusion." 





108 The Chicken Health Handbook 


Where normal microflora reside 

Bacteria are single-celled microbes that are abundant in the soil, water, and 
air. They were first discovered in the 17th century, when the microscope was 
invented. Some can move only on air or water currents; others (like salmo- 
nella) have tails that let them swim through liquids. 

Some bacteria multiply by producing spores (individual cells encased 
within a tough membrane). Others multiply by dividing themselves in half; 
under ideal conditions, they multiply so rapidly diat within hours, one bacte- 
rium becomes millions. 

Pathogenic bacteria enter the body through the digestive system, respira- 
tory system, or cuts and wounds. If they settle in an organ or tissue, the 
infection becomes chronic or long term. If they travel throughout the body by 
means of the bloodstream (a condition called "septicemia"), the infection is 
acute or short term, often ending in death. 

Bacteria produce diseases in two ways: by causing mechanical damage to 
the body and by generating toxins diat poison the body. Some bacterial dis- 
eases are caused by damage, some by poisoning, and some by both. 

Most bacterial diseases share one or more of these four properties: they 
produce carriers; they are transmitted from breeders to chicks through hatch- 

Infectious Diseases 109 



ing eggs; they are spread by rodents and wild birds; they survive for a long time 
in poultry housing. Owners of commercial flocks control bacteria by periodi- 
caily depopulating their housing and thoroughly disinfecting before bringing 
in new. clean stock (all-in, all-out management). 

Bacteria are divided into four related groups according to their shapes, vis- 
ible by magnifying them 1,000 times under a microscope. The major ones thai 
are harmful to chickens fall into three categories: 

• rod-shaped, called "bacilli," such as the organisms that cause 
colibacillosis, clostridial diseases, erysipelas, infectious coryza, 
listeriosis, cholera, pseudomonas, salmonellosis, and tuberculosis; 

• round, called "cocci," such as the organisms that cause chlamydiosis, 
staphylococcosis, streptococcosis, and mycoplasmosis (aldiough 
mycoplasmas are unique in their ability to change shape); 

• spiral, called "spirilla," such as the organisms that cause 
campylobacteriosis and spirochetosis. 

Campylobacteriosis is an intestinal disease that infects a wide range of 
animals including dogs, humans, and especially chickens. Poultry experts esti- 
mate diat 90 percent of all commercial broilers are infected. 

Several species of Campylobacter cause the disease. The species most 
likely to affect chickens, as well as humans, is C. jejuni. Campylobacters are 

1 10 The Chicken Health Handbook 

Chart 7-1 

Bacterial Diseases 





Campylobacter jejuni 



Chlamydia psittaci 

very rare 

Clostridial diseases 


Closiridum botulinum 


Necrotic dermatitis 

C, septicwn 


Necrotic enteritis 

c. perfringens 


Ulcerative enteritis 

C, colinum 



Escherichia coli 


Air-sac disease 

E, coli and other bacteria 


Chronic respiratory disease 

E. coli 



E. coli 


Swollen head syndrome 

£ coli 


Coryza, infectious 

Haemophilus paragallinarum 



F.iysipelothrix rhusiopathiae 



Listeria monocytogenes 

very rare 


Air-sac disease 

Mycoplasma gallisepticuin 


and other bacteria 

Chronic respiratory disease 

M. gallisepticuin and other 




Cholera, (acute) 

Pasteurella multocida 


Cholera, (chronic) 

P. multocida 

not common 


very rare 



Salmonella arizonae 



S. Heidelberg 

S. enteriditis 

S. typhimurium and odier spp 

very common 


S. pullorum 



S. gallinarum 



Borrelia anserina 



Arthritis, staphylococcic 

Staphylococcus aureus 



S. aureus 



S. aureus and other bacteria 



Streptococcus zooepidemicus 

not common 


Streptococcus faecalis and 

other bacteria 


Synovitis, infectious 

M. sy no viae 

not common 


Mycobacterium avium 

fairly common 

Infectious Diseases 111 

spread among chickens through infectious droppings in feed and water. The 
main symptoms are depression and watery, mucousy, or bloody diarrhea. 

No effective way has been found to treat an infected flock. 
Campylobacters are, however, particularly sensitive to drying and can be 
eliminated from housing by thoroughly cleaning and disinfecting, followed by 
leaving the coop empty for at least a week before introducing new birds. 

Clostridial diseases result from toxins produced by bacteria in the Clostri- 
diumgraup. Some clostridial bacteria do not cause disease unless a chicken's 
resistance has first been reduced by coccidiosis or by an illness (such as infec- 
tious bursal disease) that damages the immune system. 

Clostridium colinum causes ulcerative enteritis, a short-term intestinal 
disease spread by infectious droppings in litter, feed, and water. The disease is 
known as "quail disease" because it was first identified in quail, the most sus- 
ceptible of all avian species. The bacteria are able to survive under a variety of 
conditions, so once an outbreak occurs, housing is permanently contami- 
nated. Control then involves replacing litter between flocks or keeping your 
birds on wire. Ulcerative enteritis may be avoided by taking care not to bring a 
carrier into your flock. 

Clostridium septicum is commonly found in soil and in die intestines of 
chickens. It usually causes infection in combination with other bacteria, often 
after the chicken's immunity has been reduced by some other illness, espe- 
cially infectious bursal disease. Alone or in combination, the bacteria cause 
necrotic dermatitis, characterized by patches of dead skin and/or sudden 
death. Necrotic dermatitis can easily be avoided through good management 
and proper sanitation. 

Clostridium perfringens is commonly found in air, soil, water, and feces. 
The bacteria generate a potent toxin that causes necrotic enteritis in young 
and growing birds raised intensively on litter. The disease appears suddenly 
(often after a change in feed) and progresses rapidly, causing deaths within a 
few hours, sometimes without symptoms. It is easy to treat with antibiotics 
and easy to avoid through good management. 

Clostridium botulimtm, bacteria that commonly live in the intestines of 
chickens, are not themselves pathogenic. When they multiply in the carcasses 
of dead animals or in rotting solid vegetables such as cabbages, they generate 
some of the world's most potent toxins. Birds become poisoned after pecking 
at rotting organic matter or after drinking water into which it has fallen. 

A poisoned bird gradually becomes paralyzed from the feet up. Initially 
the bird sits around or limps if you make it move. As paralysis progresses 

112 Tun Chicken Health Handbook 

common name, "limberneck"). By the time the eyelids are paralyzed, the bird 
looks dead, but it continues to live until either its heart or its respiratory system 
becomes paralyzed. 

If the bird isn't too far gone, you might bring it around wiUi antitoxin (from 
a veterinarian) or by squirting cool water and an epsom salt solution into its 
crop (see "Flushes," page 192). Botulism is another disease that can easily be 
avoided through good sanitation. 


Colibacillosis is a group of infectious diseases caused by one or more 
strains of Escherichia coli, the so-called "coliform" bacteria commonly found 
in the environment worldwide. Many strains, including some that normally 
live within chickens, do not cause disease. Other strains are opportunistic. 

The illnesses caused by E. coli are varied and often complex. The bacteria 
may infect alone or may combine with or follow other diseases, especially 
chronic respiratory disease, infectious bronchitis, infectious synovitis, and 
Newcastle. A bird's susceptibility to coliform invasion is increased by stress 
and by damage to its respiratory system caused by ammonia fumes or dust. 

Coliform infections range from severe and acute to mild and chronic. The 
susceptibility of chickens varies with the bird's strain and age — infection is 
more common in young birds than in older ones. The bacteria are transmitted 
through the shells of hatching eggs, causing dead embryos or chicks widi in- 
fected navels (omphalitis). In the brooder, E. coli bacteria spread rapidly by 
means of infected droppings picked from litter, feed, or water. 

The bacteria enter a chicken by way of either the digestive or the respira- 
tory system but may eventually settle in the bird's eye, heart, liver, navel, 
oviduct, leg joints, or wing joints. They may get into the bloodstream, causing 
acute septicemia and the sudden death of an apparently healthy bird. 

Coliform bacteria survive for long periods in dry litter and dust and are 
spread through the droppings of infected rodents and chickens. Respiratory 
colibacillosis can be prevented by minimizing stress, providing good ventila- 
tion, and keeping chickens free of mycoplasmal and viral infections. Intestinal 
colibacillosis is more difficult to avoid but can be minimized by controlling 
rodents anc 


Infectious coryza is a respiratory disease caused by Haemophilus paragal- 
linantm bacteria that are prevalent in die southeastern United States and in 

respiratory diseases and often occurs in combination with them. Its chief 

Infectious Diseases 113 

symptoms are swelling of the face and, in chronic cases, the unmistakable 
odor of nasal discharge. 

Infectious coryza is spread mainly through contact with carrier birds, 
which include all survivors of the disease and other birds in the same flock, 
even though they may never have had symptoms. The disease is easily intro- 
duced by unknowingly bringing growing or mature carriers into an established 
flock. A vaccine is available, but should be used only to prevent future out- 
breaks once Infectious coryza has been diagnosed in your flock. 

The only way you can get rid of infectious coryza is by disposing of the 
infected flock, disinfecting the premises, and leaving housing vacant for at 
least 3 weeks before introducing new birds. Infectious coryza is not transmit- 
ted through hatching eggs, making it possible to start a new Hock by incubating 
eggs from infected breeders, provided you take great care to raise the chicks in 
an unconlaminated environment. 


Erysipelas, caused by Erysipelothrix rhusiopalhiae bacteria, is rare in 
chickens. It is significant as a disease chickens share with many other birds and 
animals, notably turkeys, pigs, sheep, and humans. 

Bacteria shed in the droppings of infected birds or other animals survive 
for years in alkaline soil. Chickens on range that previously held infected tur- 
keys, sheep, or pigs may become infected through open wounds that result 
from fighting, cannibalism, or dubbing. The disease is most likely to occur 
among cockerels on free range — cockerels, because they commonly wound 
each other in peck-order lights; free range, because it provides contact with 
potentially contaminated soil. 

The most startling symptom is the sudden death of apparently healthy 
cockerels, while birds in nearby flocks (on uncontaminated soil) thrive. Since 
survivors continue to shed bacteria, and since this disease poses a health risk 
to humans, the only sensible approach is to dispose of an infected flock and 
start a new flock on fresh ground. Erysipelas is not transmitted through hatch- 
ing eggs, making it possible to start a new flock by hatching eggs from infected 
breeders, provided you keep the new birds away from contaminated ground. 

Mycoplasmosis encompasses any disease caused by mycoplasma bacte- 
ria, the smallest living organisms capable of free existence. A mycoplasma is 
about die same size as a virus, but (unlike a vims) can multiply outside a living 
cell. The two important mycoplasmas affecting chickens are Mycoplasma 

fectious synovitis 

1 14 The Chicken Health Handbook 

in all ages, and M. gallisepticum, which causes air-sac disease in ) 
and chronic respiratory disease in growing and mature birds. 

Diseases caused by mycoplasmas can be difficult to recognize without 
laboratory work, since they often occur in combination with other bacteria 
and with viruses. They are spread from infected breeders through hatching 
eggs and by direct contact with infected or carrier birds. Survivors become im- 
mune to future infection but remain carriers. The bacteria cannot survive long 
away from a bird's body. 

At one time, all chickens carried mycoplasma and became infectious in 
response to stress. Today, mycoplasma-free strains are available among the 
commercial breeds. The bacteria threaten primarily commercial operations 
with high concentrations of large flocks in relatively confined geographic areas. 
The farther your flock is from an infected flock, the lower its risk of exposure. 


Chlamydia psittaci, a bacteria-like organism, affects all species of birds. It 
is like a virus in that it multiplies only within die cell of another life form, but 
otherwise it behaves like a bacteria and can be treated with antibacterial drugs. 
It produces an infection commonly known as "psittacosis" or "parrot fever" 
because it was first identified in psittacine birds (parrots). Outbreaks are cycli- 
cal and, among poultry, are more common in turkeys than in chickens, which 
are naturally resistant. Chlamydiosis is significant because it infects humans 
as well as birds. 


The genus Salmonella contains over 2,000 different species. Although Uiey 
all have the potential of causing disease in chickens, only about a dozen cause 
70 percent of the salmonella outbreaks. Evidence suggests that 75 percent of all 
chickens are infected with one or more kinds of salmonellae at some time in 
their lives. 

These bacteria create a serious problem for poultry keepers because 
chickens that appear perfectly healthy are often carriers. Symptoms may be 
triggered at any time by stress due to crowding, molting, feed deprivation, drug 
treatment, or simply being transported. 

The bacteria are transmitted by carriers to dieir offspring through hatch- 
ing eggs (a process called "transovarian" transmission) in one of two ways: 

• die yolk is infected as the egg is being formed in the body of an infected 

Infectious Diseases 115 

dirty nest; the bacteria then penetrate the shell (most likely because the 

shell gets cracked or wet) and multiply within the egg. 

An infected embiyo may die in the shell toward the end of incubation or 
may hatch into an infected chick. The disease spreads to healthy ■chicks or 

mals (including humans). It spreads by means of contaminated droppings in 
litter, drinking water, and damp soil around waterers. It is spread mechanically 
by flies, rodents, wild birds, used equipment, shoes, truck tires, and the like. 
Salmonellae may also be present in rations containing contaminated livestock 

Salmonellae generally enter a bird's body by way of mouth. They cause 
inflammation of the intestines, or Ulcerative enteritis, and so are often referred 
to as "enteric" bacteria. Acute Ulcerative enteritis is indicated by watery diar- 
rhea, sometimes smelling bad or containing blood. Symptoms of chronic 
Ulcerative enteritis are emaciation and persistent diarrhea, which may appear 
mucousy or bloody. If the disease becomes septicemic, the bird's head, comb, 
and wattles turn dark and purplish. 

Salmonella bacteria are divided into four groups with symptoms so similar 

that laboratory identification is required to tell them apart. 

U S. pullorum causes pullorum, a disease that affects only poultry, prima- 
rily chickens. Because it is always associated with diarrhea topped witii white 
urates, it was once called "white diarrhea." Pullorum is spread by infected 
breeders through hatching eggs, causing death to embryos in the shell or to 
chicks soon after they hatch. Since some states require exhibition birds to be 
blood tested, a home-testing kit is now available. Local laws may require you to 
pass an examination in order to test your own flock. 

2. S. gallinarurn causes typhoid that is also specific to poultry, primarily 
chickens. Like pullorum, typhoid is rare in North America. 

3. Paratyphoid infection (para meaning resembles) is caused by over 1 50 
different species of salmonellae thai invade a large number of animal species. 
Paratyphoid is the most important bacterial disease in the hatching industry, 
since it causes deaths among chicks and stunts survivors. This group is also 
important in die meat and egg indusUy, since it is responsible for causing food 
poisoning in humans. The most common paratyphoid strains in chickens are 
S. Heidelberg and S. typhimurium; at present, the most serious to humans is S. 

4. _S. arizonae, like the paratyphoid group, infects a large number of ani- 
mal species. These salmonellae cause avian arizonosis, mainly among turkeys. 

ment to paratyphoid. 

is similar in appearance and treat- 

1 16 The Chicken Health Handbook 

Controlling Salmonellae 

Salmonellae readily survive and multiply in the environment, making 
their control difficult. They survive for years in infected droppings, feathers, 
dust, and hatchery fluff, and for almost a year in garden soil fertilized with in- 
fected droppings. The bacteria cannot survive long at 140"F (60°C), a 
temperature well below that of healing compost. The bacteria thrive in fresh 
litter, but cannot live long in built-up litter, due to the high pH of ammonia. 

Antibiotics can be used to control a salmonella outbreak, but culling is 
preferable to treatment for at least three reasons: 

• antibiotics alter intestinal microflora, interfering with recovery; 

• the use of antibiotics causes antibiotic-resistant strains of bacteria to 

In 1935, the National Poultry Improvement Plan (NPIP) was organized to 
standardize pullorum blood-testing and eliminate reactors from breeding 
flocks. Later, tests for other salmonelloses were added to the program. Ap- 

Clean." Information on NPIP, which publishes a directory of pullorum-free 
breeding flocks, appears in the appendix. 

Avoid salmonellosis by purchasing birds from disease-free flocks and pur- 
chasing rations that do not contain slaughterhouse wastes. Keep feed and 
water free of droppings. Minimize stress. Clean and disinfect facilities between 
flocks; clean and disinfect incubators and brooders between hatches. If an out- 
rid of salmonellae unless you get rid of the carriers. 


Spirochetosis is rare in North America, although the tick that carries it is 
quite common in the Southwest. Symptoms include yellowish-green diarrhea 
containing lar ge amounts of white urates, and a high rate of deaths. Control 
the disease by controlling fowl ticks and by keeping susceptible birds away 
from birds that are immune carriers due to exposure to fowl ticks. 


Staphylococcus aureus bacteria commonly live on a chicken's skin or mu- 
cous membranes. Normally they increase the bird's resistance to other 
infections, but will themselves cause infection if they get into the body through 
a break in the skin. Procedures such as dubbing, cropping, debeaking, and toe 
clipping open the way to a staph infection. 

Infectious Diseases 117 

Staph bacteria are the most likely cause of infection in feet (bumblefoot), 
joints (arthritis), and breast blisters. Newly hatched chicks become infected 
through open navels (omphalitis). If a chicken's immune system has been per- 
manently damaged by infectious bursal disease or Marek's disease, staph may 
get into the bloodstream, causing sudden death, laying hens in hot weather 
are particularly susceptible. Ironically, mild stress increases a chicken's resis- 
tance to staph infections. 


Streptococcus bacteria normally live within the intestines of chickens, in- 
fecting bu ds only if their resistance is low — usually due to infection by some 
other disease. S.faecalisis one of the causes of omphalitis, in which embryos 
die in the shell and chicks die soon after hatching. S. zooepidemicus can cause 
sudden death in mature birds. S. equisimilis causes wounds to fill with pus. 
Avoid strep infections by minimizing stress and practicing good sanitation. 


Pasteurellosis is a group of illnesses caused by 125 species of pasteureila 
bacteria. The only significant disease nf chickens in this group is cholera, 
caused by Pasteureila multocida, a bacterium that bodi causes damage and 
generates toxins. 

Fowl cholera can be eidier acute or chronic. Although the two forms are 
quite different, symptoms may overlap, since survivors of the acute form often 
become chronic. Mature chickens are more susceptible than young ones. 

P. multocida bacteria survive at least 1 month in droppings, 3 months in 
decaying dead birds, and 2 to 3 months in moist soil. They are spread primarily 
through mucus discharged from the mouth, nose, and eyes of infected birds 
(including wild species), wild animals (rodents, raccoons, opossums), live- 
stock (particularly pigs), pets, and humans. They may be eaten in 
contaminated feed or water and may be spread on contaminated equipment 
and shoes. They are not transmitted through hatching eggs. 

Antibiotic treatment sometimes reduces the rate of death, but die disease 
usually returns when medication is withdrawn. At one time, cholera was very 
common. Today it is controlled through good management, which entails not 
bringing in older birds diat might be carriers and not mixing birds of different ages. 


Avian tuberculosis, one of the first poultry diseases ever investigated, is 
caused by Mycobacterium avium, bacteria that infect all species of birds, but 

118 The Chicken Health Handbook 

more often chickens and captive exotic birds tiian other domestic poultry or 
wild species. The bacteria also infect pigs and rabbits, and to some extent 
people (although a different bacterium is usually responsible for human TB). 

Avian tuberculosis is more likely to be found in the northcentral states 
than in the West or South. It spreads through contact with the droppings of 
infected birds. The bacteria survive in soil for up to 4 years. The concentration 

and on how crowded they are. 

Since the disease requires a long period of exposure to get established, it 
affects primarily older birds. Symptoms are not dramatic. An infected chicken 
is less active than usual and gradually loses weight, even though it continues to 
eat well. Eventually its breast muscles shrivel, causing its keel to stick out. It 
may live for months or years, depending on how extensively the disease in- 
vades its body. 

Prevention entails replacing each year's breeding or laying flock with 
young birds, keeping birds away from housing or range that formerly held an 

picking in their droppings. 

The disease may be controlled by blood-testing or skin-testing a flock and 
removing positive reactors. If just one infected bird is overlooked, however, the 
disease will continue to spread. Since contaminated premises are difficult to 
decontaminate, the best approach is to dispose of an infected flock and estab- 
lish a new flock in a new environment. 

Some bacteria commonly found in the poultry environment infect chick- 
ens only if their resistance has been reduced by some other disease or 
condition. Once chickens become infected, the bacteria multiply within the 
birds' bodies, become more numerous in the environment, and continue to 
cause disease. Among these opportunistic infections are two that are signifi- 
cant in their ability to infect humans as well as chickens. 

Listeria monotytogenesbacxeria are common in the soil and intestines of 
birds and other animals living in temperate climates. They cause listeriosis, a 
disease to which most chickens are resistant. The bacteria primarily infect a 
chicken's heart and brain (encephalitic form), but may get into die blood- 
stream (septicemic form) and cause death. 

Pseudomonas aeruginosa bacteria live in soil, water, and other humid en- 
vironments. Infection may occur in chickens treated with a vaccine or 
antibiotic that has been handled in an unhygienic manner. Pseudomonas 
spreads from breeders to chicks through hatching eggs, causing death to 

Infectious Diseases 1 19 

Viral Diseases 

Compared to bacteria, viruses are simpler in structure and are much smaller. 
They are, in fact, the smallest padiogens known — so tiny they can be seen 
only through a microscope that magnifies diem to 100,000 times. Like bacte- 
ria, not all viruses cause disease and the diseases they do cause range from 
mild to fatal. 

Viruses differ from bacteria in being more host specific. They are more dif- 
ficult to control than bacteria because they 

• break down the defenses of a healthy bird, 

• do not respond readily to drugs, 

• survive well in nature, 

• are readily transmitted from one location to another. 

Since they are so small, millions of viruses can travel on one speck of dust, 
lust think how many can be carried on the hair of a fly, a rat's foot, a feather, the 
sole of a man's shoe, or a used chicken crate. 

Outside the cells of another living organism, a virus has no life — it neither 
breathes nor eats. Its only known activity is to take over the cell of another life 
form for the purpose of making copies of itself. 

Pathogenic viruses usually get into a chicken's body by being inhaled or 
swallowed, but they may also enter through an eye or a wound (including an 
injection puncture). Sometimes viruses invade a cell and hide there for 
months or years before becoming active. Sometimes they take over cells near 
their point of entry, causing a skin disease such as pox. Other times diey travel 
to another preferred site, most often the respiratory system (infectious bron- 
chitis) or die nervous system (Marek's disease). Sometimes they travel through 
the bird's body, producing plague-like infections such as exotic Newcastle dis- 
ease and lethal forms of avian influenza. 

Viruses cause disease in five ways, by 

• disrupting or destroying cells; 

• invading or disrupting the immune system; 

• activating the immune system, causing fatigue or fever; 

• triggering development of antibodies that lead to inflammation or 
dssue damage; 

• interacting with chromosomes to cause a minor. 

Usually when a bird is attacked by a virus, its immune system mobilizes to 
fight off the virus, which may take a few days to a few weeks. In die process, the 
bird's body becomes sensitized to the virus, and it is thereafter immune to the 
disease caused by that virus. The bird may, however, continue to shed the virus 
and infect birds that haven't yet been exposed. 

120 The Chicken HeAWH Handbook 








Viruses Infecting Chickens 

infectious anemia 
egg drop syndrome 

infectious bronchitis 


Newcastle disease (mild) 
Newcastle disease (exotic) 

epidemic tremor 



very rare 

infectious bursal disease common 


infectious laryngotracheitis common 

very common 


very rare 


Infectious Diseases 121 

Virus Family 

Chicken Disease 


Reo virus 



arthritis rare 
infectious stunting syndrome rare 

lymphoid leukosis 
ranting syndrome 

rotaviral enteritis 

very rare 


* Illustrations are drawn to scale. 

Some viruses, on the other hand, attack so fast the bird's body cannot re- 
spond before serious damage or death occurs. Other viruses weaken the 
immune system, leaving the bird open to attack by an opportunistic or sec- 
ondary infection (which may cause the bird's death). If a chicken has a viral 
infection when it is vaccinated against some other disease, the virus may inter- 
fere with die vaccine's ability to trigger immunity. 

Viruses are classified into families according to their size and shape. Each 
family includes numerous members, and new families are constantly being 

Adenovirus Syndromes 

Viruses In the adenovirus family are not yet well understood. They appar- 
endy cause a variety of infections, often in combination with other organisms. 
They may be the cause of infectious anemia, a fata] disease of broiler chicks 
intensively raised on used li Iter. The viruses enter a chicken's body through die 
digestive system and spread slowly by means of contaminated body dis- 
charges, especially droppings. Their main method of transmission is through 
hatching eggs laid by infected hens or placed in contaminated cartons. Iodine 
disinfectant slows die spread of disease. Chicks are protected by maternal an- 
tibodies for their first 2 or 3 weeks of life. 

Egg drop syndrome is caused by a waterfowl adenovirus introduced to 
chickens eidier through vaccine derived from infected duck eggs or through 
contact with infected waterfowl or drinking water contaminated by them. The 

virus remains quiet and undetected until hens approach their peak of produc- 
tion. Eggs laid by infected hens may have thin gritty shells, soft shells, or no 
shells. The first sign in brown-egg layers is pale eggs. Although the virus has 
been found in numerous ducks and geese in North America, and has infected 
chickens elsewhere, so far no chickens have experienced egg drop syndrome 
in North America. 

Viral arthritis, caused by the avian reovirus, is quite similar in appearance 
to infectious synovitis caused by mycoplasma bacteria. The main symptoms 
are swollen hocks and lameness, primarily in intensively raised broilers 4 to 8 
weeks old. Aside from vaccination, the only known way to prevent viral arthri- 
tis is to avoid overcrowding. 


Infectious bronchitis, the most contagious disease of chickens, is a respi- 
ratory illness caused by a coronavirus and characterized by coughing, 
sneezing, and rattling sounds in the throat. It starts suddenly, spreads rapidly, 
and can travel through the air to a second flock more than 1 ,000 yards away. 
Deaths occur primarily in chicks. Pullets that survive may have permanent 
ovary damage and may not lay eggs as mature hens. 

Vaccination is not foolproof, since it bestows immunity only against the 
strains contained in the vaccine, and new strains keep popping up. Survivors 
are carriers, so the only sure way to get rid of infectious bronchitis is to get rid of 
your flock, clean up, disinfect, and start over. Because the disease is not usually 
transmitted through hatching eggs, you can get clean chicks from an infected 
flock, but be sure to carefully clean up the environment and avoid introducing 
infected birds in the future. 

Bursal Disease 

Infectious bursal disease occurs when a birnavirus invades lymph tissue, 
particularly tissue of the cloacal bursa. The disease is sometimes called 
"Gumboro disease" because it was first studied in Gumboro, Delaware. It 
causes atrophy of the cloacal bursa, resulting in suppressed immunity and 
greater susceptibility to future infections, particularly colibacillosis and ne- 

an immune response to vaccines. 

The disease appears suddenly, usually in large flocks of broilers, and in- 
volves most birds in the flock. The first symptoms are watery or whitish 

Infectious Diseases 123 

diarrhea that sticks to vent feathers, causing birds to pick at their own vents. 
Deaths, when they occur, peak within a week and survivors recover rapidly 
thereafter. A subsequent infection in the same housing may be so mild you 
don't notice it. 

IBD virus is not egg-transmitted and survivors are not carriers, but the dis- 
ease is highly contagious and difficult to get rid of in housing that once held an 

natural immunity. Vaccines ar e also available. 

Viral Diarrhea 

Enteritis, characterized by inflamed intestines and diarrhea, has many vi- 
ral causes, some of which have yet to be discovered. Viral enteritis in chickens 
is becoming more common than ever, and can be divided into three main 

Bluecomb — cause unknown. The disease affects pullets just coming into 
production. It is similar to bluecomb in turkeys, caused by a coronavirus to 
which chickens are resistant. 

Infectious stunting syndrome — cause unknown, but likely involves one or 
more reoviruses. This disease primarily infects intensively raised broilers. 

Rotaviral enteritis— rotaviruses are common in the poultry environment 
and do not always cause disease. When infection does occur, massive amou nts 
of new viruses are released in the droppings of infected birds, causing the dis- 
ease to spread. 

Avoid viral diarrhea through good sanitation and not crowding birds. 
Thoroughly clean up and disinfect between flocks, and don't reuse old litter. 


Avian encephalomyelitis is a relatively rare infectious disease of chicks 
caused by a picornavirus. Its chief symptoms are loss of coordination and 
rapid trembling of the head and neck, giving the disease its common name, 
epidemic tremor. The disease is transmitted from breeders to chicks through 
hatching eggs. An adult outbreak is so mild it is likely to go unnoticed, lasts less 
than a month, and leaves birds immune without making them carriers. Survi- 
vors of a chick outbreak should be culled, since they rarely develop into good 
layers or breeders. 

Avian influenza was among the first diseases known to be caused by a vi- 
rus. It is caused by several different orthomyxoviruses and comes : 

124 The Chicken Health Handbook 

forms, ranging from mild to rapidly fatal. Symptoms vary widely and may 
relate to respiration (coughing, sneezing), digestion (appetite loss, diarrhea), 
reproduction (reduced fertility, soft -shelled eggs), or nerves (twisted neck, 
wing paralysis). Sometimes the first symptom is numerous sudden deaths 
of apparently healthy birds. 

In North America, outbreaks among chickens are rare and widespread 
in both time and place, and primarily affect operations where large numbers 
of chickens are concentrated. If avian influenza occurs in your area, stay 
away from infected flocks and their handlers. If possible, keep your flock 
indoors, away from wild birds that can spread the disease. In the event of a 
serious outbreak, you may be advised to vaccinate your flock to help locally 
contain the disease. 


Infectious laryngotracheitis, or "laryngo," is a highly contagious 
respiratory disease caused by a virus in the herpes family. Its chief symptoms 
are moist respiratory sounds (gurgling, choking, rattling, whistling, or 
"cawing") and coughing up bloody mucus. In a serious case, a large 
percentage of birds die. 

Vaccination keeps the disease from spreading, but causes birds to 
become carriers. Vaccinating therefore doesn't make sense unless laryngo 
is prevalent in your area. Vaccination is usually recommended for those 
who show or who regularly bring in adult birds, but since vaccinated birds 
are carriers, if you vaccinate, you run die risk of having your birds infect 
any unvaccinated birds they come into contact with. (In the old days, flocks 
were immunized by bring in an infected bird - survivors of the ensuing 
infection became immune.) 

The virus does not live long off birds and is not spread through hatching 
eggs. You can safely start a new flock from infected breeders if, and only if, 
you dispose of the old flock and carefully clean and disinfect housing before 
moving the young birds in. 

Newcastle Disease 

Newcastle disease gets its name from the British town of Newcastle- 
upon-Tyne, one of the first places where it was studied. The disease comes 
in many different forms, ranging from mild to devastating. Mild forms are 
quite common, not particularly serious, and can be controlled by vaccination 
where the virus is prevalent. Virulent or so-called "exotic" forms will infect 
even a properly vaccinated flock, but fortunately are relatively rare. 

Vaccination in the face of an exotic outbreak slows the spread of disease 
and reduces the number of deaths, but won't keep birds from getting the 

Exotic Newcastle is usually introduced by illegally imported cage birds 

Infectious Diseases 125 

that have not gone through official quarantine. It is spread by contaminated 
droppings on used equipment and the shoes of humans, and causes a rapid, 
high number of deaths. The disease can easily be confused with other serious 
respiratory infections. 

Symptoms include a sharp drop in laying accompanied by breathing diffi- 
culties, soon followed by muscular tremors, twisted neck, and wing or leg 
paralysis, and sometimes watery, greenish diarrhea. If an exotic infection oc- 
curs in your area, stay away from infected birds and keep their handlers away 
from your flock until the outbreak has been controlled. 

Chart 7-3 

Forms of Newcastle Disease 




Formal Name 


Beaudeltes affects all ages, 
mild respiratory 

Hitchner's affects young birds, 
mild to serious 
respiratoiy infection 


mild intestinal 

drop in laying, 
slight wheezing 
few deaths 

some deaths 


Newcastle disease 

Newcastle disease 

asymptomatic - 
enteric lentogenic 
Newcastle disease 




affects all ages, 
acute, lethal, 
nervous & 

affects all ages, 
acute, lethal 
respiratory & 
intestinal infection 

appears suddenly, 
gasping & coughing, 
drop in laying, 
wing or leg paralysis, 
100% affected, 
up to 50% adults die, 
up to 90% young die 

sudden death or 
listlessness, rapid 
breathing, drop in 
laving, watery greenish 
diarrhea, 100% affected, 
nearly 100% die, bloody 
digestive tract 

velogenic Newcastle 

velogenic Newcasde 

126 The Chicken Health Handbook 


Pox in chickens (nol at all the same as chicken pox in humans) occurs 
when the pox virus gets into wounds caused by insect bites, dubbing, fighting, 
cannibalism, or injury on poorly designed equipment. Fowl pox appears in 
two forms: diy pox affecting the skin (cutaneous form) and wet pox affecting 
the upper respiratory tract (diphtheric form). 

Dry pox causes clear or whitish bumps on the comb, watdes, and odier 
unfeatiiered portions of the body. The bumps eventually come together to 
form scabs, fall off, and leave scars. Wet pox causes yellowish bumps in the 
mouth, throat, and windpipe, sometimes affecting the bird's ability to breathe 
so that it dies from suffocation. In either case, survivors recover in 4 to 5 weeks. 

In pox-prone areas, disease may be controlled through vaccination and by 
controlling mites and mosquitoes. 

Viral Tumors 

Some viruses are nearly identical to the growth -promoting chromosomes 
in a chicken's cells, and have the ability to invade cells and modify those chro- 
mosomes. The resulting mutation induces the cells to multiply out of control, 
causing a tumor. 

Tumors can occur in any part of a chicken's body. They may be benign 
(starting and developing in one place) or malignant (spreading to other parts 
of the body). External benign tumors may be removed surgically (assuming the 
bird is worth the cost); malignant tumors usually come back after surgery. In- 
terior tumors, whether benign or malignant, are rarely discovered until after 
the bird dies. 

In veterinary jargon, a tumor is called a neoplasm (from neo meaning new 
and plasm meaning shape). Miscellaneous viruses occasionally cause neo- 
plasms in a hen's ovary or oviduct (most often in hens over one year old) or 
along the backs and thighs of broilers (appearing as crater-like ulcers that may 
clump together). 

By far the most important tumors in chickens are in the avian leukosis 
complex, an interrelated group of viral diseases that affect few other birds (or 
animals) besides chickens and that fall into two categories based on their 

• Marek's disease, caused by six different herpesviruses that primarily 
affect the nerves of growing birds; 

• the leukosis/sarcoma group (leukosis means "whitening," sarcoma 
being a malignant tumor), caused by retroviruses tiiat primarily affect 
older birds. 

Infectious Diseases 127 

Marek's Disease 

The Marek's virus kills 
more chickens than any 
other disease. It's so com- 
mon, you can safely assume 
your flock is infected, even if 
your chickens don't show 
any symptoms. Stress due to 
crowding, moving, or even 
the natural process of ma- 
turing can weaken a flock's 
immunity, causing an out- 
break of the dormant virus. 
The virus attacks various 
parts of a chicken's body, re- 
sulting in an array of 
symptoms — droopy wing, 
paralyzed leg, head held low, 
twisted neck, blindness, sud- 
den death. 

The virus is not transmitted by means of hatching eggs. In fact, a newly 
hatched chick is briefly protected if its dam transmits a high antibody level 
through her eggs. Chicks should be brooded away from adult birds, however, 
since the first few weeks of life are the most critical time for infection. Chicks 
that are isolated until the age of 5 months develop a natural immunity that 
helps them overcome exposure to Marek's virus as adults. Some chicken 
strains are genetically more resistant titan others. 

Turkeys carry a non-tumor-forming vims that prevents the Marek's virus 
from developing tumors. Chickens that are run with turkeys therefore develop 
some measure of immunity (although keeping the two together creates other 
problems, such as the possibility of the turkeys getting blackhead from Lite 

Marek's vaccine for chicks is derived from the turkey virus, making it one 
vaccine that does not cause a mild case of disease in order for birds to build up 
antibodies. To become immune, chicks must be exposed to the turkey virus 
before they are exposed to Marek's virus. Vaccination should therefore occur 
as soon after hatch as possible and chicks should be isolated until immunity 
develops in about a week. A single vaccination confers lifelong immunity, but 
is not 100 percent foolproof — about 5 percent of all vaccinated chickens get 
the disease anyway. 

Marek's disease in chickens has been used as a model for studying cancer 
in humans, and Marek's vaccine has become a model for developing a human 

Chart 7-4 

Forms of Marek's Disease 

Form Characteristics 

Cutaneous (skin form) enlarged feather 


Neural (nerve form) progressive paralysis 
weight loss 

labored breathing 

few or insignificant 
postmortem findings 
Ocular (eye form) graying, shrunken iris 

irregular-shaped pupil 

Visceral(internal organs) tumors in ovary, heart, 

lung, and other organs 

128 The Chicken Health Handbook 

cancer vaccine. There is no evidence, however, diat the Marek's virus causes 
cancer in humans. 


Like Marek's disease, the neoplasms in the leukosis/sarcoma group infect 
all chickens by die time diey reach maturity. Rarely, however, do they cause 

The viruses in diis group are most likely to cause lymphoid leukosis, occa- 
sionally osteopetrosis (thickening of the leg bones that affects primarily 
cockerels and cocks), only rarely erythroid leukosis (causing enlarged, bright 
red liver and spleen) or myeloid leukosis (causing chalky white internal tumors 
along the spinal column and beneatii the keel). The latter two are so infrequent 
that they warrant only brief mention. 

Lymphoid leukosis usually strikes chickens just reaching maturity. The 
symptoms ar e not particularly dramatic and are so similar to those of Marek's 
disease thai the two are easily confused. Unlike Marek's disease, lymphoid 
leukosis cannot be prevented by vaccination. 

Chart 7-5 

Differences Between Lymphoid Leukosis and Marek's Disease 






Incubation period 

14 weeks 

2 weeks 

Earliest age 

14 weeks 

4 weeks 

Usual age 

over 6 months 

under 6 months 

Peak age 

4 to 10 months 

2 to 7 months 

Peak age for deaths 

24 to 40 weeks 

10 to 20 weeks 




Eye tumors 



Skin tumors 



Nerve tumors 



Liver tumors 



Heart tumors 



Intestinal tumors 



Bursal tumors 



Muscle tumors 



iKFEcnous Diseases 129 

Runting Syndrome 

Ranting syndrome, like lymphoid leukosis, is caused by a retrovirus and 
can be easily mistaken for Marek's disease. The virus that causes runting syn- 
drome seems to be more prevalent than the disease, but since it doesn't always 
produce symptoms, it's considered relatively rare and not much is known 
about it. In North America, it is most likely to occur in southeastern states, es- 
pecially Florida, Mississippi, and North Carolina. 

Fungi are parasitic plants that lack chlorophyll and live on decaying organic 
matter. They include molds, mildews, yeasts, mushrooms, and toadstools. Of 
more than 100,000 different species, most are either beneficial or harmless. 
Two kinds of fungi cause disease — yeast-like and mold-like. They cause dis- 
ease of four types: 

• allergic reaction to inhaled spores in moldy litter; 

• poisoning due to toxins released by fruiting bodies (i.e. poisonous 
mushrooms and toadstools); 

• poisoning clue to toxins generated through invasion of stored feed (e.g. 
aflatoxicosis or ergotism) — this type of poisoning is called 
"mycotoxicosis" (discussed on page 140); 

• infection due to invasion of skin, lungs, or other body dssue (e.g. favus 
or thrush) — this type of infection is called a "mycotic disease" or a 


Mycoses are grouped according to whether they are: 

• superficial — affecting the skin or mucous membranes (e.g. favus); 

• deep — affecting internal organs, usually die lungs (e.g. aspergillosis, 
dactylariosis, histoplasmosis, thrush). Deep infections are opportunis- 
dc, taking advantage of a chicken's low resistance due to stress or the 
presence of some odier disease. 

Fungal infections have gotten more common since the use of antibiotics 
became widespread, because antibiotics destroy normal body flora, making it 
easier for pathogenic fungi to lake over. Still, mycoses are rare enough in chick- 
ens that methods for their control and treatment remain less advanced than 
those for bacterial and viral diseases. 

130 The Chicken Health Handbook 

Chart 7-6 

Fungal Diseases 






Aspergillus spp 
Dactylaria gallopava 
Microsponim gallinae 
Hisioplasma atpsulatum 
Candida albicans 

very rare 

very rare 





Aspergillosis refers to any disease caused by the spores of Aspergillus spp 
fungus commonly found in the environment, especially in soil, grains, and de- 
caying vegetative matter including litter. These molds are capable of infecting 
all birds, more commonly turkeys than chickens. They produce a form of 
pneumonia diat is acute in chicks and chronic in mature birds. 

Infection is rare in North America and may easily be prevented through 
good sanitation (especially in the incubator and brooder), avoiding moldy 
grain and litter, periodically moving feeders and waterers or placing them on 
droppings boards, providing good ventilation to minimize dust, and keeping 
stress to a minimum. 

Candida albicans causes thrush or candidiasis in many species of birds 
and animals, including humans. Thrush probably occurs among chickens 
more often tiran we know, since its symptoms are not particularly distinctive. 
Thrush is primarily a disease of chicks and growing birds. It can be prevented 
by controlling coccidiosis and by avoiding the overuse of antibiotics. 

Rare Mycoses 

Uncommon fungi that occasionally invade chickens include: 

Microsponim gallinae that causes a superficial infection called "favus," in 
which the comb of a mature cock looks like it's been sprinkled with flour; 

Dactylaria gallopava in moldy sawdust used as litter, causing a brain dis- 
ease called "dactylariosis" that makes chicks tremble and walk in circles; 

Histoplasma capsulaiuin, a fungus that causes histoplasmosis, a rare but 
potentially fatal disease chickens share with other birds and with humans liv- 
ing along the Mississippi, Missouri, and Ohio rivers. 


Infectious Diseases 131 

A syndrome is a group of symptoms that occur in combination and appear as a 
particular disease. In most cases, die disease is poorly defined — its symptoms 
are not always the same and /or its cause is not yet known. These diseases are 
so poorly defined that one disease may have several names (malabsorprion 
syndrome, pale bird syndrome, infectious stundng syndrome) or the same 
name may be applied to more than one disease (e.g. runting syndrome). The 
diseases in this group are described more fully in chapter 15: 

• air-sac syndrome (air-sac disease) 

• egg drop syndrome 

• fatty liver syndrome 

• infectious anemia 

• infectious stunting syndrome 

• runting syndrome 

• star-gazing syndrome (epidemic tremor) 

• sudden death syndrome 

• swollen head syndrome 

Diseases of Unknown Cause 

Syndromes are not alone among diseases for which we've not yet found a 
cause, despite all our modern technology. The following conditions (described 
in chapter 15) have unknown causes: 

• bluecomb 

• broiler ascites 

• cropimpacdon 

• gout (visceral) 

• round heart disease 

• twisted leg 


THE ENVIRONMENT CANNOT BE OVERLOOKED as a source of health prob- 
lems for chickens. Extremely cold weather can lead to frostbite. Steamy 
weather can cause heat stress. Crowded conditions often lead to cannibalism. 
Unsafe chemicals or vegetation cause poisoning. Rodents spread diseases 
and, on occasion, attack chickens. Happily, each of these problems can be 
avoided dirough awareness and good management. 


All chickens can tolerate quite a bit of cold weadier, provided you see that their 
drinking water doesn't freeze and their housing is neither drafty nor damp. 
Draftiness removes warm air trapped by ruffled feathers. Moisture in the air 
makes chickens cold by absorbing body heat. Combs and wattles are therefore 
more likely to freeze in damp housing than in dry housing. 

Since cocks don't sleep widi their heads tucked under a wing, as hens do, 
cocks are more likely than hens to have their combs and watdes frozen when 
temperatures dip during the night. Cocks widi large combs are more likely 
than others to be frostbitten. 

Frozen combs and watdes look pale. If you discover the condition while 


Environment-Related Problems 133 

ihe part is still frozen, apply a damp, warm cloth (105T, 40.5°C) to the frozen 
part for 15 minutes or until it thaws. Do not rub. After the part has thawed, 
gently apply an antiseptic ointment such as Neosporin. Isolate the bird and 
keep an eye on it to see that the comb heals properly. 

Frozen combs and wattles are more likely to be discovered after they have 
thawed and become red, hot, swollen, and painful. The bird doesn't feel like 
moving, is listless, and loses interest in eating. If the part has already thawed, 
warming it is no longer necessary. Gently coat the part with Neosporin and 
isolate die bird. 

After the swelling goes down, the skin may peel, the part may itch, and it 
may be sensitive to cold for a while. It may turn scabby, develop pus, and even- 
tually fall off. The suffering cock will continue to lose weight and may become 

If the comb or wattles were seriously frozen, instead of swelling they may 
remain cold, begin to shrivel, and eventually die back. Other chickens may 
peck at die affected part, making matters worse. 

If a comb or watde turns black, the affected tissue has died and gangrene 
has set in — the comb or wattle is no longer receiving a blood supply and must 
be surgically removed. 

Dubbing and Cropping 

Surgical removal of the comb (dubbing) and wattles (cropping) is done for 
one of several reasons: 

• to remove injured or infected tissue 

• to keep combs and watdes from freezing 

• to increase egg production and reduce feed costs 

134 The Chicken Health Handbook 

• to minimize blood loss in fighting cocks 

• because show regulations require it 

Modern and Old English game cocks must be dubbed and cropped in or- 
der to avoid disqualification from some shows (other breeds may be 
disqualified if they oredubbed or cropped). Fighting cocks are dubbed to mini- 
mize blood loss due to injuries. In cold climates, large-combed hens may be 
dubbed to minimize heat loss, thereby reducing feed costs and improving egg 
production; cocks are dubbed to avoid frostbitten combs and watdes that in- 
terfere widi fertility. 

Dubbing and cropping are stressful and should be avoided immediately 
before or after birds are vaccinated. Neither should breeders be dubbed before 
or during hatching season, or low fertility may result. Birds can be dubbed at 
any age after their combs and watdes develop, but those in the 8- to 12-week- 
old bracket bleed less than older birds. 

Regardless of a bird's age, it can bleed to deatii as a result of improper dub- 
bing. Feeding each bird a vitamin K tablet daily for 5 days preceding the 
operation aids clotting. The surgery is painful and should be done under vet- 
erinary supervision so an anesthetic can be used. 

Use small tin snips or 6-inch (12 cm) curved surgical scissors, available 
from a medical supplier, and heat the instrument to destroy any bacteria that 
might be present. Snip off the comb V z inch (1 cm) above the head. Cauterize 
the surface by searing it with a hot iron to minimize bleeding. If the wattles are 
to be cropped at the same time, snip diem off and coat them with an astringent 
such as iron subsulfate. 

To prevent infection, either inject % cc penicillin into the bird's breast 
muscle daily for 10 days or add 1 teaspoon (5 ml) tetracycline or baci tracin per 
gallon to tite drinking water for 10 days. The comb and wattles should heal 
within 30 days. 

Heat Stress 

Lightly feathered breeds like Leghorns, Hamburgs, and Minorcas suffer less in 
warm weather than heavily feadiered breeds like Brahmas, Cochins, Rocks, 
and Reds. Laying hens are more susceptible to heat stress than birds not in 
production. Closed nests make matters worse. Avoid using trapnests during 
hot weather. If hens must be trapnested, check nests frequently and release 
hens before they suffocate in the close confines of a too-hot nest. Outdoors, 
white birds are less subject to heat stroke than dark birds because they reflect 
sunlight better. 

Any chicken's body operates most efficiently when the outside tempera- 
ture is 70-75°F (21-24'C). Chickens cannot sweat to keep cool. Instead, they 


hold their wings away from their bodies and pant. Holding the wings away 
from the body exposes more skin surface under the wings, thereby increasing 
evaporation and radiational cooling. Panting releases heat through evapora- 
tion from the lungs. 

A mature chicken starts panting when the temperature reaches 85°F 
(29.5"C). A chick pants when die temperature is 100°F (38°C) or more. Panting 
causes a chicken to exhale large quantities of carbon dioxide, which raises its 
blood pH. The resulting changes in physiology cause stress. The chicken stops 
eating and lays fewer and smaller eggs with thinner shells. A young bird stops 

When the temperature reaches 104"F (40°C), even panting is not enough 
and deaths may occur. Cool things down by increasing air circulation — open 
doors and windows or install a fan. Among the least expensive fans is a vari- 
able-speed paddle or Casablanca fan. Be sure the coop is properly vented so 
hot air doesn't get trapped against the ceiling. 

Hosing down the outside walls and roof improves cooling duough evapo- 
ration, as does occasionally misting or fogging chickens. Take care not to mist 
so much that water puddles on the floor. Mist only adult chickens and only 
when the temperature is above 95"F (35"C) and the humidity is below 75 per- 
cent. Cooling won't occur if the air is already so humid that no more water can 
evaporate. Mist only when the fan is running or air circulation is otherwise suf- 
ficient to dry the birds. 

Chickens eat less when they're hot. To ensure adequate nutrition, feed 
only fresh rations. Chickens also drink more in hot weather so they can expel 
extra moisture in their droppings as an additional cooling mechanism (caus- 
ing droppings to be looser in hot weather). Encourage drinking by supplying 
cool water and extra watering stations. If the water supply remains the same 
when a flock's water requirements go up, water deprivation may result (see 
"Dehydration," page 40). 

Walking among your birds will encourage them to move, stimulating 
drinking, but don't disturb them at peak heat periods, which only increases 
stress. Symptoms of serious heal stress include drinking excessive amounts of 
water, labored breathing, and weakness. If a heat-stressed bird becomes pros- 
trate, but is still alive, move it into the shade. Dunk it in cool water and use a 
plastic tube attached to a funnel to fill its crop with cool water. If the bird sur- 
vives, it may remain weak for several days. 


Light, high-strung laying breeds, especially Leghorns and other Mediter- 
raneans, are more likely to engage in cannibalism than the heavier American 
and Asiatic breeds. Within a breed, some strains are more cannibalistic than 

1 36 The Chicken Health Handbook 

others. Birds of the same strain may be cannibalistic when raised in one place 
but not another, proving that you can discourage cannibalism by providing a 
proper environment. 

y causes, of 

• heat without adequate ventilation 

• nests not dark enough 

• bright lights in the brooder house (lights on all night or sunlight 
coming dirough windows) 

• crowding (especially in fast-growing chicks that quickly fill the avail- 
able space and can't get away from each other) 

• boredom ( 
in free-ranged flocks) 

• feed and water troughs too few or too close together (failure to increase 
the number of feed and water stations as chicks grow) 

• feed too high in calories and too low in fiber (chickens quickly satisfy 
their nutritional needs and get bored) 

• external parasites (a chicken pulls out its own feathers, drawing blood 
that attracts other birds to pick) 

• injury or bleeding (e.g. from an injured comb or a broken feather quill) 

Toe Picking 

Cannibalism often starts with toe picking, a common problem among 
chicks, especially those reared on paper to prevent litter eating. Toe picking 
can also occur in chicks brooded on wire — sharp wire edges cut their toes and 
the bleeding attracts toe pickers. Toe picking may start when chicks can't find 
anything else to eat because the feeder is poorly designed, is too high, is too far 
away, or is too small for the number of chicks involved. 

To get chicks picking at feed instead of feet, sprinkle a little starter ration 
on paper, or place shallow containers of starter close to the heat source where 
the chicks can easily find it. If toes are injured from picking, light the brooder 
with a red light so chicks can't easily delect blood while the toes heal. 

Head Picking 

Head picking generally occurs in older birds, especially when combs or 
watdes bleed due to fighting or frostbite. Cocks or hens housed in adjoining 
cages may pick each other's heads, even if the birds have been debeaked. 
When possible, space cages far enough apart to prevent picking. Cardboard or 

Environment-Related Problems 137 

hiivt'c i 

rier reduces air circulation, causing caged birds to suffer in warm weather. Iso- 
late any bleeding bird until the wound heals. 

Feather Picking 

Evidence of feather picking is dull, broken feathers and bare patches on a 
, breast, back, and below the vent. Tail-feather picking is especially 
common in growing birds, when new feadiers filled widi blood attract pickers 
before enough plumage grows to cover the area. But it can start at any time, 
triggered by crowding, lack of exercise, irritation due to parasites, or low- 
protein diet and other nutritional deficiencies. Picked birds must continually 
grow new leathers, causing the same stress reactions associated with molting, 
including a drop in laying. 

Feather loss doesn't necessarily indicate feather picking. Layers often have 
broken or missing feathers, especially on their necks and tails, nibbed off on 
feeders and nests. Mating cocks frequently wear the feathers off a hen's back. 
The annual molt also causes feather loss. Some birds drop and replace their 
feathers gradually, others lose many feathers at a time. During the molt, en- 
courage feather growth and discourage feather picking by increasing dietary 

Vent Picking 

Vent picking is the worst form of cannibalism because it escalates quickly 
and often ends in death. It can start if nests are too light, so that a hen's vent 
gets picked while she's laying. But it is most likely to occur among pullets just 
coming into lay, usually after one tears tissue or prolapses while passing an 
unusually large egg (see "Prolapsed Oviduct," page 53). 

Egg Eating 

Egg eating occurs when not enough nests are provided, nests are too light, 
housing is too light in general, or hens are crowded and bored. Egg eating is 
also encouraged by anything that causes egg breakage — eggs aren't collected 
often enough, have soft or thin shells, or become cracked due to insufficient 
nesting material. Once chickens find out how good eggs taste, they will break 
eggs on purpose to eat them. 

A nutritional deficiency, especially vitamin D or calcium, can cause soft 
shells that lead to egg eating. A laying hen's calcium needs are increased by 
warm weather and by age. Appropriate nutritional supplements include free- 
choice feeding of limestone or ground oyster shell, or adding vitamin AD&E 
powder to drinking water three times a week. 

140 The Chicken Health Handbook 

Toxic seeds are sometimes accidentally harvested along with feed grains. 
Such seeds include: 

• coffee weed {Cassia obntsefolia) in corn and soybeans, causing a drop 
in egg production, diarrhea, paralysis, and death; 

• gossypol in cottonseed meal, causing bluish combs and wattles, 
emaciation, low egg production, and low egg quality; 

• crotalaria seeds and stems, causing bright yellowish -green droppings 
and inactivity; 

• sorghum seed, causing depressed growth and leg deformity; 

• iye seed, causing poor growth, pasting, soft bones, and lameness. 

Other naturally occurring toxins in die environment cause selenium poi- 
soning (see page 32), blue-green algae poisoning (see "Algae Poisoning," page 
246), botulism (see "Clostridial Diseases," page 1 1 1). and mycotoxicosis. 


Unlike infectious fungal diseases, which occur when fungi or their spores 
invade body tissue, fungal poisoning occurs when chickens consume toxic by- 
products generated by mold growing in feed. A number of poisons or 
mycotoxins are produced by molds that grow naturally in grains, and some 
molds generate more than one kind of poison. 

Aspergillus flatus, the same fungus that causes aspergillosis, also causes 
aflatoxicosis, a disease that increases a bird's susceptibility to heat stress and 
infection. In die United States, anatoxins are the only feed-borne mycotoxins 
regulated by law. 

Fusarium sporotrichioides, along with other species of Fusarium, causes 
fusariotoxicosis. a digestive disorder that interferes with egg production, 
growth, and feathering. 

Clai'iceps purpurea produces a highly toxic alkaloid that causes ergotism, 
the oldest known mycotoxicosis. It is characterized by shriveled combs, sores 
on legs, convulsions, and death. 

Aspergillus spp and other fungi generate ochratoxin, one of die most poi- 
sonous of all mycotoxins. The fungi that cause ochratoxicosis prefer high 
temperatures and so, in contrast to ergot and fusarium molds, they thrive in 
pelleted feed (which is manufactured under intense heat) unless it contains 
mold inhibitors. 

All mycotoxicoses increase a chicken's need for vitamins, trace elements 
(especially selenium), and protein. Poisoning is difficult to identify and diag- 
nose, in part because one feed source may contain more than one kind of 
mycotoxin. A posidve diagnosis usually requires analysis of the feed to identify 

any fungi present. Since small-flock owners generally buy feed in small quanti- 
ties, it's likely that a given batch will be used up before anyone thinks of 
analyzing it. Once the contaminated feed is removed, chickens usually re- 

rungal poisoning can be avoided by using commercially prepared feeds 
containing mold inhibitors and by storing feeds away from humid conditions. 
Use plastic storage cans rather than metal ones, which generate moisture by 
sweating. Never give chickens feed lhathasgone moldy. If you buy moldy feed, 
take it back and insist on a refund. 

Fungal Poisoning 



Caused By 

Aspergillus flavus and other 

Clavkeps purpurea 

Grain Source 

all grains 

wheal, rye, cereal grains 

Fnsariotoxicosis Fusariuni sporolridiioicles and corn, wheat, barley, millet, 

Ochratoxicosis Aspergillus ochraceous and 
other fungi 

barley, com, sorghum, wheat 

Antifreeze Poisoning 

Nearly all animals are attracted to ethylene-glycol because it tastes sweet 
and it doesn't freeze, thereby becoming the only "water" available to drink in 
cold weather. Poisoning is most likely to occur due to antifreeze spillage in fall, 
winter, and early spring. The lethal dose is 0.1 ounce per pound (8 ml /kg) of 
body weight, or about 3 tablespoons of antifreeze per mature chicken. 

Antifreeze destroys a bird's liver and kidneys. The bird appears drowsy 

droppings. It ruffles its feathers, lies down, and dies. Few people would recog- 
nize antifreeze poisoning unless they actually saw the bird drinking antifreeze. 

Chick Poisoning 

Chicks are especially susceptible to certain toxins, including: 

carbon monoxide, from being transported in the poorly ventilated 
trunk of a car (chicks die); 

144 The Chicken Health Handbook 

Rats are active at night. If you see a rat in the daytime, you have a bad rat 
problem — the rals have overpopulated and the dominant ones are keeping 
the weaker ones away from feed, forcing them to eat during the day. 

Feed loss is one of the worse consequences of an infestation. Eight rats eat 
1 pound (2.2 kg) of feed each day. One pair of rats produces four to seven litters 
each year. Even though not all of the offspring reach breeding age, within a 
year one pair can easily become 1 ,500 rats. 


Chickens are the natural enemies of mice, but the agile little rodents are 
good at scurrying away. Mice reproduce even faster than rats — each pair has 
five to eight litters per year. Mice are most active at dusk and dawn, but they 

Rodent Control 

Despite all our modern technology, we still haven't found a better mouse- 
trap. The best way to discourage rodents is to make the chicken house 
unattractive to them. Since rats and mice shun open areas, keep the land 
around your coop clear of weeds and trash. If die floor is raised, make sure it's 
at least 1 foot (30 cm) above ground so rodents don't feel protected. Use hang- 

-Reiaied Problems 145 

ing feeders that are difficult for rodents to reach, store feed in containers with 
tight-fitting lids, and avoid spillage. 

Keep a cat. A cat's advantage for rodent patrol far outweighs any disadvan- 
tages it may have as a potential disease carrier. 

If you have a serious rodent problem, set traps. Use spring traps, placed at 
right angles to the wall with the trigger and bait close to wall. Since mice run 
along sills, rafters, and other high places, set traps high as well as on the 
ground. As cliched as it may sound, Swiss cheese is still the best trap bait. 

Identify tunnels and fill them in. Place poisoned bail near tunnels that are 
reopened within a day or so (the unopened tunnels have become inactive). 

active tunnels. Rebait any that are opened again. Continue until tunnels are no 
longer reopened. 

Rodent Bait 

The most common rodent poison contains an anticoagulant that com- 
petes with vitamin K and thereby interferes with blood clotting. A 
multiple-dose anticoagulant must be eaten several times to be effective. A 

2 IN. t/~ 
(5 CM|-k^ 

Rodent bait station 


2 FT. 
(61 CM| 


r\ I FT. 

(31 CM). 


146 TttE Chicken Health Handbook 

single-dose anticoagulant kills after 
only one feeding. 

Since a multiple-dose bait requires 
several days to take effect, be sure to put 
out enough bait to accomplish your 
purpose. Keep the bait out until no 
more is eaten. Multiple-dose bait is 
relatively safe for pets and other ani- 
mals, since a single dose is ineffective. 

Single-dose anticoagulants are also 
relatively safe for other animals, since a 
large dose is needed to be lethal to ani- 
mals larger than a rodent. Even though single-dose anticoagulants require 
only one feeding, leave the bait out for at least 2 days to make sure all rodents 
consume some. 

Not all baits are anticoagulants. Some contain vitamin D3, which causes 
death through an imbalance of blood-calcium levels. This type of bait is fairly 
safe to animals other than rodents, since they must eat a large amount to 
be affected. Single-dose bait that attacks the nervous system is toxic to all 

Regardless of a bait's level of safely, take care when putting it out so that 
chickens, pets, and children can't get into it. Never just scatter bait around or 
drop it into tunnels — rodents may kick it out where chickens or other animals 
will find it and eat it. No bait is effective if an abundance of other feed is avail- 
able, so carefully clean up spilled grain before putting out bait. 

Chart 8-4 


Multiple-Dose Single-Dose 



Unlike other baits (which are relatively 
safe), Bromethalin affects the central 
nervous system and is fairly toxic to all 

Diagnostic Guides 

TRYING TO FIGURE OUT WHAT DISEASE yoiir chickens have, or diagnosing 
the disease, involves four basic steps: 

• examining flock history 

• considering the symptoms 

• conducting a postmortem examination 

• performing laboratory procedures 

Home laboratory procedures are pretty much limited to investigating in- 
ternal parasites, as described in chapter 5. Postmortem examination is 
discussed in detail in the next chapter, as is the process of submitting speci- 
mens to a pathology laboratory. Consider enlisting the help of your state lab if, 
after going through the first three steps, you're still not sure what disease 
you're dealing with. 

Flock History 

When you experience a problem, suddenly all those little details you thought 
you'd never forget, but now can't quite remember, become immensely impor- 
tant. You'll be happy you took a few moments to write down events as they 
occurred. If you neglected to keep accurate records as you went along, try to 
reconstruct your flock's history based on the accompanying chart. 


148 Tin; Chicken Health Handbook 

Chart 9- 1 

Flock History 


Other diseased flocks 
Previous diseases 

Flock age 
Time of year 
Feed changes 
Duration of disease 
Rate of spread 
Past vaccinations 
Medications used 
Percentage involved 
Mortality rate 

Can Help You Determine This: 
Diseases prevalent in your area 

Disease-causing agents already present on your property 

Diseases possibly transmitted by carrier chickens, visitors, 
dirty equipment, etc. 

Diagnosis based on age group involved (approximation only) 

Relationship to weather or to carriers such as mosquitoes 

Diseases due to improper nutrition or toxins in feed 

Diagnosis based on how long symptoms last 

Diagnosis based on how fast symptoms spread 

Diseases not likely to be involved 

Diagnosis based on flock response to drugs 

Diagnosis based on percentage of sick birds 

Diagnosis based on percentage of dead birds 

Chart 9-2 


Signs of Health 

Body Pa rt 


Comb & wattles 

bright, full, waxy 


bright, shiny, alert 


clean, no rasping 

Head & tail 

held high 


full & plump 


firm but not hard 


erect, active, alert 


smooth & clean 


clean, slighdy moist 


firm, gray-brown 

with white caps 

Symptoms are visible signs of disease. 
In order to readily recognize symp- 
toms, you need to be thoroughly 
familiar with how a healthy flock looks, 
acts, and smells. Be observant when 
you tend your flock. Each time you en- 
ter your coop, stand quietly for a 
moment and watch. 

Any change you detect, including a 
change in the amount of feed your 
birds eat, the amount of water they 
drink, their posture, their droppings, 
and the condition of their plumage may 
all be first signs of disease. 

Signs of Disease 

If you notice anything unusual in your flock, follow these steps in checking 
for signs of disease. 

1. Watch from a distance to see what each bird is doing, how it moves, and 

Diagnostic Guides 149 

Taking Blood Samples 

Your veterinarian orpathologist may askyou to bring in blood samples from live 
birds. Blood samples are usually taken from a main wing vein or brachial. Begin 
by pulling a few feathers from the depression in the upper part of the underside 
of the wing to expose the main vein. Disinfect the skin with 70 percent alcohol. 

In one hand, hold both wings over the chicken's back so it can't flap. Insert 
a sharp 20-gauge needle ( 3 /i-inch for chicks, 2-inch for mature birds) into the 
vein with the needlepointingaway from the chicken's body and toward the wing 
tip. Starting with the plunger pulled back slightly to allow an initial air space in 
the syringe, slowly but steadily pull back on the plunger until the syringe 
contains at least 2 ml of blood. 

I Take care to neither go through the vein nor nick the vein at the top, both 
of which will prevent you from drawinga sample. The first timeyou need a blood 
sample, try to get a veterinarian or other experienced person to show you how. 

When you withdraw the needle, if the bird bleeds internally, press the spot 
wi tli your tiiumb for a few moments. U nless the chicken has a clotting problem, 
drawing blood should pose no threat to its health. 

Without jostling or rotating the syringe, place it in a clean container where 
it will remain horizontal. Do not refrigerate or freeze it, but take the sample to 
the lab for analysis the same day it was drawn. If the lab needs a whole blood 
sample (rather dian one in which water-like serum separates from the blood) 
your veterinarian or pathologist will give you an anticoagulant to keep the blood 
from separating. 

150 The Chicken Health Handbook 

how it stands when still. Check droppings on the ground. Note unusual smells. 
Listen for unusual sounds: if you whistle, the birds will stop their activities to 
listen, and you can more easily hear respiratory sounds. 

2. Count the number of affected birds. Come back a few hours later and 
count again. How fast the illness sweeps or creeps through a flock can provide 
an important clue as to what the disease might be. Since different diseases 
progress at different rates, if more than one disease is involved, how fast indi- 
vidual symptoms move through a flock can be especially important. 

3. Keep track of the number of birds that die. Note how and where they 
die, and how soon they die after they first show symptoms. 

4. For a closer look, catch birds with a minimum of fuss. Symptoms can 
change when you pick up a bird, especially if die bird had to be chased to be 
caught. Check body openings for unusual excretions: discharge from the 
moudi, clogged nostrils, sticky eyes, diarrhea. Note any unusual smell coming 
from these discharges. 

5. Check for wounds, swellings, blindness, and external parasites. (See 
chapter 4 for instructions on checking for parasites.) To check for blindness, 
move a finger toward the bird's eye. If the bird blinks, it is not blind. Don't wave 
your hand, or air movement may make the bird blink. 

6. If symptoms lead you to suspect a disease that involves a change in 
body temperature, take the bird's temperature: shake down the thermometer, 
insert it into the bird's vent, and hold it there for 3 minutes or until the ther- 
mometer beeps if its electronic. The normal temperature for an adult bird is 
103°F (40"C); normal body temperature for a chick is 106.7°F (42'C). 

7. Use the diagnostic charts in this chapter to help you identify the dis- 
ease. Then look up each possibility in the alphabetic list in chapter 15 (or, in 
the case of parasites, chapters 4-6) and find the condition whose combination 
of symptoms most closely matches those of your flock. 

Matching Symptoms to Diseases 

General symptoms appear in nearly any illness, whether it results from an 
infection, parasitic invasion, nutritional deficiency, or poisoning. General 
symptoms include droopiness, ruffled feathers, weight loss, and reduced egg 

Each disease group has its own set of general symptoms as well. Coughing, 
sneezing, and labored breathing are general symptoms of respiratory diseases. 
Diarrhea, increased thirst, and dehydration are general symptoms of intestinal 
diseases. Inability to stand or walk are general symptoms of muscular or skel- 
etal disorders. Twitching, trembling, and convulsions are general symptoms of 
diseases that attack the nervous system. 


Diagnostic Guides 151 

with reddish, bad smelling nasal discharge is specific to infectious coryza. 
An inflamed foot with a hard, swollen abscess is specific to bumblefoot. Dis- 
tended abdomen and an unhealed or mushy navel in a newly hatched chick is 
specific to omphalitis. 

Your chickens may not have all the symptoms listed in chapter 15 under 
the disease you suspect, or your flock may have symptoms in addition to those 
listed. Some diseases are caused by different strains of the same pathogen, af- 
fecting different birds in different ways. Some pathogens affect different birds 
in different parts of their bodies. Diseases may occur in combinations of two or 
more, causing a confusing array of symptoms. 

Veterinarians arrive at a probable diagnosis (otherwise known as an edu- 
cated guess) in part by considering the accumulation of symptoms. The rest of 
us are more likely to work by the process of elimination — decide what the 
problem is not, and you may eventually determine what it probably is. 

Start with the obvious. Consider management errors causing your birds to 
run out of feed or water, get too hot or too cold, become injured, or be attacked 
by a predator. If your chickens seem a little droopy or they aren't growing well, 
they most likely have worms, external parasites, or coccidiosis. Before you start 
considering rare diseases, eliminate common diseases as the probable cause. 


To some extent, diseases can be diagnosed by the appearance of a bird's 
droppings. But remember, variations in droppings are quite normal. Light 
brown (or sometimes copper green), pasty droppings, usually bad smell- 
ing, are normal cecal droppings deposited by each chicken two or three 
limes a day. 

Chickens don't usually produce liquid urine, as humans do. Instead, they 
expel solid urine in the fonn of salts or urates that look like chalky white caps 
on top of their droppings. An excessive amount of urates can be a sign that the 
kidneys are not functioning properly, perhaps because the chicken isn't get- 
ting enough to drink or has a kidney disease. 

Watery droppings are a sign of increased urine output. They often appear 
as a pool of liquid surrounding solid matter that's slightiy greenish in color, 
and can occur when chickens eat lots of succulent spring grass or drink extra 
water during warm weather. Watery droppings can also be a sign of disease 
caused by such things as kidney failure and fever. 

Intestinal diseases often cause diarrhea. Based on the specific disease in- 
volved, the diarrhea may be foamy, bloody, sticky, pasty, mucousy, 
off-colored, smelly, or any combination thereof. 

152 The Chicken Health Handbook 
Chart 9-3 

Diseases Causing a Change in Droppings 





0-10 days 
0-3 weeks 

0- 4 weeks 

1- 6 weeks 

2- 6 weeks 

3- 14 weeks 

3- 18 weeks 

4- 6 weeks 
4-12 weeks 

12 weeks + 

up to 5 weeks 

chicks and 



Growing & 

vent pasting 

vent pasting 

watery diarrhea 
white or greenish brown 

diarrhea with undigested 



whitish or water diarrhea, 
may be bloody 

bloody diarrhea 

diarrhea (may be bloody) 
white-capped greenish 


watery diarrhea with pasting 

bloody diarrhea 

profuse, watery diarrhea 
white droppings, sometimes 

greenish yellow diarrhea erysipelas 

pasted vent 



infectious stunting 

necrotic enteritis 

infectious anemia 

infectious bursal 


ulcerative enteritis 
infectious synovitis 



coccidiosis (cecal) 
rotaviral enteritis 

watery, mucousy, pasty, tan 

or bloody diarrhea 
green diarrhea 
diarrhea, sour crop 

mucousy, bloody diarrhea 
yellowish droppings 


chronic respirator)' 





not common 


not common 









6 mondis + 

loose white or green 

lymphoid leukosis 


Diagnostic Guides 153 






greenish, watery, pasty 






diarrhea, first watery and 

cholera (acute) 

not common 

& mature 

white then greenish yellow 

Mature hens 


fatty liver syndrome 

not common 


waterv. greenish. 

Newcastle (exotic) 

verv rare 

blood-stained diarrhea 

yellow, watery, foamy 



1 1 i"t"ri i_i *i 

U till 1 1 lea 

yellowish or greenish- 



yellow diarrhea 

yellow diarrhea 


not common 

green diarrhea 



2 years + 

persistent diarrhea 




prppnish-vellow diarrhea 


\ i i i i t j 1 1 y vi i * 


OTPpnish-vfllovv diarrhea 

"snirochf* tori's 


cannpd With while 

chalky white 

oviduct flukes 


greenish diarrhea 



foamv diarrhea 


verv common 

v i v \_/ 1 1 1 1 1 ivy i i 

blue or green fluorescent 

nioldv grain 

noi common 


bripht vpIIow prpen 

crnlpilnri;! *ipr>d 

ra rp 




rve seed noisonini' 



coffpp-wppH ^ppH 

1 Cll c 






V-X t LI I I 1 1 1 - * 

1 ! 1 - 1 1 | 'I ' 1 1 ! 1 ! 1 i 1 1 





watery diarrhea 

antifreeze poisoning 

not common 

brown, pasty, smelly 

none — normal cecal 




loose, watery droppings 

none — cooling 


mechanism in hot 


154 The Chicken Health Handbook 

Chart 9-4 

Diseases Interfering with Movement 





At hatch 

0- 3 weeks 

1- 3 weeks 

1-8 weeks 
1-12 weeks 
3-6 weeks 

3-20 weeks 

3- 18 weeks 

4 weeks 

4- 8 weeks 
4-10 weeks 
4-12 weeks 

4-17 weeks 

Chicks & 


backward somersaulting congenital tremor 

uncoordinated, circling 
inability to stand 
droopy wings, draggy legs 

leg paralysis, twisted neck 

jerky movements, falling 

lost balance, 
outstretched legs 

flapping wings, Hipping 
onto back, death 

squatting, feet up, weight 
on hocks 

lameness, incoordination 


degenerated leg muscles 



lameness, swollen hocks 
and feet 

weight on keel, 
reluctant to move 


fatty liver syndrome 

Newcastle (exotic) 


epidemic tremor 



very rare 



encephalomalacia rare 

sudden death 

kinky back 

necrotic dermatitis 

infectious bursal 

not common 


white muscle disease not common 

viral arthritis 
run ting syndrome 
infectious synovitis 


not common 

cryptosporidiosis not common 

6 weeks + lameness, swollen joints cholera (chronic) not common 


lameness, weakness 
circling, twisted neck 
unable to stand, twisted legs rickets 
and wings 

circling, head twisted back toxoplasmosis 
one or both legs bent twisted leg 


lameness, swollen joints erysipelas 




Diagnostic Guides 155 






I ■ rnunti n 

nrnnnif unnrf ("it*Qrrfr\/ 1 oil 

uiuujjy wing, uiaggy 

IMpiai*"*^^ 1 1 P 

twisted neck 

twisted legs with swollen 

slipped tendon 





abscess on foot pad 





inability to stand 

cage fatigue 

not common 

inability to stand 


not common 


wing or leg paralysis 

Marek s disease 


Young or 

lameness, stilted gait, 




thick leg bones 

lameness, swollen hocks 



n « #-l root 
dllU led 

ytiltpH 0*11! thif*L*pnpH Ipu^ 

qphIv Ipo mitp 

VCIy LUJlllllUIl 

weakness, paralysis 


not common 


fowl tick 


N /I *j 1 1 1 
LVlctLUl C 

llClIlUlo, IWlblCU Mill'. 

IMcWLdJtUC \CaU11L; 

very i are 

n;ir3l\r7Pfi wino nr Ipo 

lameness, neaa rremors 


not common 


convulsions, paralysis 

algae poisoning 


progressive flaccid 




swollen joints 




swollen, white foot joints 

gout (articular) 

not common 

weak legs, lost coordination 



leg deformity 

sorghum seed 




rye seed poisoning 


incoordination, twisted neck 

antifreeze poisoning 

not common 

156 The Chick-en Health Handbook 



Other characteristics 



small eggs, low hatchability 



35% drop 


cholera (chronic) 

increase in blood spots 

not common 

chronic respiratory 

coughing, weight loss 



coccidiosis (intestinal) 

thin breast, weak legs 


egg drop syndrome 

in brown-egg layers 
15-30% drop for 2 weeks 


epidemic tremor 

temporary drop 



70% drop 


tatty iii/er syndrome 

sudden drop 




sudden drastic drop 


infectious coryza 

watery' eyes, swollen face 



temporary drop 




suuQcn aiop, orooanicss 


lymphoid leukosis 

tumors in ovary 



temporary drop 

often no other symptoms 


pox (dry) 

bumps on combs & wattles 

not common 

swollen head syndrome 

swollen head & wattles 



prominent, deformed keel 


water deprivation 


infectious bronchitis 

very low production 


Newcastle (exotic) 

very low production 



Newcastle (exotic) 

very rare 

cholera (chronic) 

wrinkled, off-color yolks 

not common 

cholera (chronic) 

low production 

not common 

no other symptoms 


vitamin A deficiency 

clutches farther apart 

not common 


drop in production 


salt deficiency 

drop in production 

not common 



Diagnostic Guides 157 

in Eggs 


Othpv rhnvnctpri^tia 


Misshapen Newcastle (exotic) 

very low production 

very rare 


infectious bronchitis 

very low producnon 


Pale shells 

egg drop syndrome 

low production 



vitamin D excess 

leave holes if scraped off 

not common 



infectious bronchitis 

very low production 



Soft shells egg drop syndrome 

low production 


infectious bronchitis 

veiy low production 



low production 



low production 


vitamin D deficiency 

cycles of low production 

not common 

Thin shells 

cage fatigue 

soon stop laying 

not common 

egg drop syndrome 

shells are gritty 



high death rate 


infectious bronchitis 

very low production 



yellow diarrhea 


No shells 

egg drop syndrome 

egg eating 



low production 


No eggs 

cage fatigue 

followed by paralysis, death 

not common 


no other symptoms or death 


Newcastle (exotic) 

drop within 3 days 

very rare 

gout (visceral) 

soon followed by death 


infectious bronchitis 

gasping, coughing 


158 Ti tB Chicken Health Handbook 

Age Characteristics Disease Prevalence 


gasping, sneezing, "chirping" 
labored breathing, droopy 

Newcastle (exotic) 

very rare 

0-1 week 

gasping, swollen eyes 



0-4 weeks 




1-7 weeks 

swollen eyes and sinuses 

roup (nutritional) 


4 weeks + 

nasal discharge, swollen face 

infectious coryza 


4-12 weeks 

slight rattling 

infectious synovitis 



4-17 weeks 




5-12 weeks 


air-sac disease 


6 weeks + 

sneezing, ratding, nasal 

cholera (chronic) 




rapid labored breathing 




hrpathirip riifficiiltv 
nasal discharge 



Growing & 

rapid breathing, mucus 
discharge mouth and nose 

gasping, ratding, coughing, 
bloody mucus, nasal 

cholera (acute) 





gasping, coughing 
difficult breathing, nervous 

Newcastle (exotic) 


very rare 


nasal discharge 
gasping, ratding, wet eyes 
coughing, sneezing, rattling 
sneezing, progressive swelling 
of head and wattles 

infectious bronchitis 
swollen head 





Diagnostic Guides 159 

Chart 9-7 

Diseases Causing Discoloration 





1-4 weeks greenish blue breast and legs 

1-6 weeks pale skin 

3-12 weeks reddish black skin patches 

3- 14 weeks pale comb, wattles, skin, legs 

4- 6 weeks dark face 
4- 1 2 weeks bluish comb 

4-17 weeks pale skin 

6 weeks + bluish, hot comb 

Chicks & 

Over 6 months 

Growing & 
mature cocks 

Growing & 



Maturing & 


Mature Hens 

2 years + 

darkened head 
pale, shriveled comb 
black feathers in red or buff 

pale, shriveled, sometimes 
bluish comb 

grayish white patches 
on comb 

darkened head 

pale head 
bluish comb 

pale skin 
pale head 

blackish, swollen eyes 

draining straw-colored fluid 
purplish head, comb, wattles 
pale, shriveled comb 
bluish comb 

pale, swollen comb and 

darkened head and shanks 

pale or bluish comb and 

exudative diathesis 

infectious stunting 

necrotic dermatitis 

infectious anemia 

infectious synovitis 


cholera (chronic) 



chronic respiratory 



Marek's disease 
cholera (acute) 

Newcastle (exotic) 











lymphoid leukosis common 





very rare 

paratyphoid common 
pullorum rare 
aspergillosis (chronic) rare 

fatty liver syndrome not 


gout (visceral) common 
tuberculosis common 

(chart continues oner) 

160 The Chicken Health Handbook 

Diseases Causing Discoloration (cont.) 




bluish, wilted, cold comb 



bluish comb and wattles 

gossypol seed 



pale comb, skin, shanks 




pale head 




darkened head, comb, and 




white bumps on comb and 

pox (dry) 




pale or purplish comb 



Chart 9-8 


Diseases Causing Off Odors 

Characteristics Disease Prevalence 

Hatched chicks 

Chicks & 


Maturing pullets 

Growing & 
mature cocks 

Growing & 


smelly unabsorbed yolk sac omphalitis common 

smelly mouth discharge canker rare 

distended, sour crop thrush rare 

sour crop bluecomb rare 

moldy smelling, scabby comb favus rare 

smelly nasal discharge infectious coryza common 

smelly droppings on vent 

pasted vent not 


sour-smelling, distended crop crop impaction rare 

Diagnostic Guides 161 

Diseases Affecting the Eyes 





0-1 week 

swollen with yellow cheesy 

aspergillosis (acute) 



1-3 weeks 

dull eyes 

epidemic tremor 


1 -8 weeks 

one or both eyes blind 



4 weeks + 

one or both eves swollen shut 

infectious coryza 


I In in S wppI'^ 

one or both eyes swollen or 

nn i£trvnhnin 


' < . ■ i . ' 1 1 


rhnlpra frhrnniH 

CllUICld i III 1 . 





i at c 

swnllf n pvpliHs with stirkv or 

'.li' H LyvllUo Willi * i 1 1 P . \J 1 

roup (nutritional) 


piippsv fiisf'lif-n'Pf 4 




vji owing of 

trotny eyes 

ClllUIllL 1 EbJJIldUJI V 

L.U1 1 II 1 1UI 1 




sunken eyes 




Maturing & 

mucousy eyes 

cholera (acute) 





watery, swollen eyes 




clear eye becomes blind 


l/UI 1 1 1 1 IU 1 1 


cloudy eye 



cloudy eye, sunlight avoidance conjunctivitis 

wateiy eyes 

infectious bronchitis 


watery and/or swollen eyes 



cloudy grayish, dilated, 

Marek's disease 


irregular pupil; distorted 

or blinded eye 

blackish eyes draining 

Newcastle (exotic) 


straw-colored fluid 

red swollen eyes 

swollen head 

very rare 


swollen, inflamed, watery 

eye worm 



162 The Chicken Health Handbook 

Chart 9-10 

Diseases Causing Sores in the Mouth 





Chicks & 

white or yellow sores 





whitish yellow sores 

roup (nutritional) 


grayish white circular sores 




yellow patches on roof 

Newcastle (exotic) 

very rare 

sores at corners of mouth 


very rare 

white, yellow, or brown 




sores in roof of mouth 

red mites 


Chart 9- 11 

Diseases Causing Temperature Changes* 


» 1 1 1 H- 1 (11,1 i I / / I 



3-18 weeks 

fever, then drop to below 

infectious bursal 




4-12 weeks 

hot, swollen legs and feel 

infectious synovitis 

not common 

6 weeks + 

hot, bluish comb 

cholera (chronic) 

not common 

12 weeks + 

1-5 "F (1-3°C) above normal 



Young or 

warm, puffy legs 





fever, weakness 




hot, inflamed foot 





body feels cold 




Maturing & 


cholera (acute) 

not common 



fever, depression, weight loss 


not common 

fever, purplish head 




hot swollen joints 

staphylococcic arthritis 


fever, weight loss 



fever, sneezing, rattling 



fever, dropping to below 



normal just before death 

fever, pale head, diarrhea 



*The normal body temperature for adult chickens is 103'F (39.5'C): for chicks, it's 106.7"F 

Diagnostic Guides 163 

Chart 9-12 

Diseases Causing a High Rate of Death 





0- 3 weeks rapid deat hs 

diarrhea, leg paralysis 
diarrhea, gasping 

1- 3 weeks jerky movements, falling over 
3-18 weeks diarrhea, vent picking 

Over 3 weeks growing thin while eating well 

2- 6 weeks reluctant to move, diarrhea 

3- 6 weeks can't walk, dehydration 

3- 20 weeks huddling, ruffled feathers 

lameness, loose feathers & skin 

4- 6 weeks no symptoms or droopiness 
4-17 weeks reluctant to move 

Up to 5 weeks droopy, thirsty, huddling 

Young & bloody diarrhea 

growing gasping, watery nose and eyes 

weakness, rapid deaths 
diarrhea, inflamed vent 
emaciation, incoordination 

Growing diarrhea, nasal discharge, 

cockerels lameness 

Growing slow growth, diarrhea 

diarrhea, sour crop 

Broiler niffled feathers, slow growth 


Maturing sour crop, diarrhea 

Maturing & rapid death 

mature coughing, gasping 

Mature thin-shelled eggs 

depression, weight loss 

Any convulsions, paralysis 

progressive flaccid paralysis 
ruffled fea tliers, no appetite 

carbon monoxide 


epidemic tremor 

infectious bursal 

Marek's disease 

necrotic enteritis 

kinky back 

infectious anemia 
necrotic dermatitis 




coccidiosus (cecal) 

rotaviral enteritis 



broiler ascites 


cholera (acute) 




algae poisoning 



not common 





not common 

not common 


not common 








not common 

very rare 
not common 


(chart continues over) 

164 The Chicken Health Handbook 

Diseases Causing a High Rate of Death (cont.) 

Age Symptoms Disease Prevalence 

Any (cont.) sudden death gout (visceral) not common 

coughing, huddling influenza rare 

respiratory problems &/or Newcastle (exotic) very rare 

paralysis &/or sudden 


bumps or scabs on face, mouth pox (wet) rare 

lameness, diarrhea, rapid deaths pseudomonas rare 

diarrhea, weakness, convulsions spirochetosis rare 

Chart 9-13 

Diseases Causing Sudden Death 




At hatch 



1-12 weeks 

jlUUUvU UvBUl oy 1 Ivll v*l 1 It* 

foul mnn 

0—4 wf(*ks 

ni illon i in 

1 /LI 1 11/ 1 11 1 1 1 


3—1 4 Weeks 

iiifprrioim anpnii;-i 

II liUv L- 1* J U O Lll 1 \ 1 1 1 Ht 

lint cniVimon 

3-20 weeks 

necrotic dermatitis 


2-6 weeks 

necrotic enteritis 


4-12 weeks 

ulcerative enteritis 


4-8 months 

round heart disease 

very rare 

WVCI OIllUlllllS 

iviiipiioiu leukosis 





Broiler cockerels 

broiler ascites 


Maturing pullets 



Growing & mature 





Mature hens 

fatty liver syndrome 

not common 



not common 





not common 


not common 



gout (visceral) 



very rare 



Marek's disease 


Newcastle (exotic) 

very rare 

choking (too rapid eating) 

not common 

pesticide poisoning 

not common 

anaphylactic shock 


Postmortem Examination 

MANY DISEASES, in addition to causing easily observable symptoms, cause 
less obvious changes inside the body. Studying the insides of a bird lor signs of 
disease is called postmortem examination ("post" meaning after and 
"mortem" meaning death). 

Conducting a postmortem is sometimes called "posting," or more scien- 
tifically, "necropsy" (the animal equivalent of an autopsy). Posting gives you 
clues to help you determine the cause of a disease outbreak. 

Laboratory Analysis 

If you have a sudden, severe disease outbreak, or you find several dead birds in 
a short time, the best way to get a rapid, positive diagnosis is to have a few birds 
posted at your state poultry pathology laboratory (you'll find a list of state labs 
in the appendix). Since the pathologist will want to know the disease's progres- 
sion, submit either three live birds in various stages of illness or one bird diat 
has recently died, one that is very sick, and one just beginning to show symp- 

When you bring live birds to the lab, be prepared to leave them behind. 
The pathologist will not help you try to save any birds you bring in for examina- 
tion. Taking chickens to the lab is a one-way street for two reasons: 

• A pathologist's job is to examine a bird's innards, which means die bird 
must be dead before the examination can proceed. 


1 66 The Chicken Health Handbook 

You wouldn't want to return a bird lo your flock after it has been 
exposed to all the disease-causing organisms floating around the 


Submitting Specimens 

When you plan to submit a dead bird for examination, as soon as you find 
one dead, wet its feathers with cold water and a little detergent, taking care not 
to get any into die mouth or nose. Bag the bird in plastic and refrigerate it until 
you're ready to leave for the lab. Whedier you're submitting dead or live birds, 
identify each with a numbered leg band (or wrap a piece of tape several times 
around its leg and write a number on it with an indelible marker). 

Write a detailed history of the disease, how it affected each bird you are 
submitting, and anything else about your chickens you think might be impor- 
tant. The lab will provide a form for you to fill out. Attach your history to the 

If the lab is far from your home, you may wish to ship your birds. Call first 
for shipping instructions. It's a good idea to call ahead, anyway, instead of jusl 

Disease History 

When you submit a sample to a diagnostic laboratory, provide this 

• your name, address, and phone number 

• housing type (cage, floor, range) 

• feed used (sources and types) 

• breed of your birds 

• number in your flock 

• birds' age(s) 

• where you got them 

• symptoms you have observed 

• approximate number sick 

• number that have died 

• when, where,: 

any medications you have tried 

recent changes (new rations, new chickens brought in, toxic spray- 
ing in your area, etc.) 

additional history (vaccinations, nearby flocks, previous disease 
problems, etc.) 

Postmortem Examination 167 

erinarian and get a referral to the lab. If there are no veterinarians nearby, or 
your vet is not willing to examine chickens, say so. 

Unfortunately, most veterinarians know little about chickens. Even if 
you're lucky enough to find one with poultry experience, the fee you will be 
charged may be more than the cost of buying new, healthy birds. State poultry 
pathology laboratories, on the odier hand, charge little or nothing for an initial 

What to Expect 

Within a few days, the pathologist should call you with a preliminary re- 
port, then follow up with a written report. Don't be bashful about asking 
questions if you don't understand something — pathologists tend to use 
words only a veterinarian or other trained person can understand. If you sub- 
mit your birds under a veterinarian's referral, your vet will explain the report to 

report is inconclusive, the pathologist may take an educated guess as to what 
the problem might be and ask if you want the diagnosis confirmed by further 
laboratory tests such as tissue examination, bacterial cultures, virus isolation, 
or sensitivity tests (to determine which drug, if any, will kill the particular 
padiogen in question). These tests can be time-consuming and expensive. 

Even if die diagnosis is certain, the pathologist is unlikely to suggest a spe- 
cific treatment. The job of a pathologist is to identify diseases, not recommend 
treatments. You should, however, be given enough information to obtain de- 
tails on treatment options from your veterinarian, your state Extension poultry 
veterinarian, or your state Extension poultry specialist. Armed with this infor- 
mation, you can decide whether to treat the remainder of your chickens or get 
rid of them and start over. 

Do-It- Yourself Posting 

Running to the path lab with every dead bird you find is neither feasible nor 
even necessary. A 5 percent death rate is considered normal in any flock. Still, 
it's a good idea to examine dead birds and record the results in your flock his- 
tory. You may see an emerging pattern drat can help you discover and treat a 
disease in its early stages of development. 

Eveiy flock includes weak birds that have lower resistance than others to 
disease as a result of stress, genetic factors, or insufficient nourishment due to 
being far down in the peck order. These weaker birds become indicators of 
impendingproblems. If you do find signs of a disease in progress, you can take 

168 The Chicken Health Handbook 

future samples to a qualified pathologist for a con- 
firmed diagnosis. 

Anotiier reason to do your own posting is diat, if 
die lab is particularly busy, the pathologist may not 
get back to you for several days or even weeks. 
Meanwhile, if your chickens are getting sicker or are 
dying fast, you might tentatively identify the prob- 
lem yourself and take appropriate action. The lab 
report, when it comes, will then serve as a confirm- 
ing diagnosis. 

Posting a chicken makes sense only if you know 
what the insides of a healthy bird look like — some- 
thing you can easily learn by paying attention when 
you butcher chickens for eating. The more often 
you post chickens, the more observant you will be- 
come. To help sharpen your skills, get a good reference book of color photos, 
such as Color Atlas of Diseases and Disorders of the Domestic Fowl and Turkey 
or the less expensive Soluay Manual of Poultry Diseases (both books are listed 
in Recommended Reading, page 333). 


If you suspect a 
chicken of having 
chJamydiosis or any 
other disease that is 
contagious to hu- 
mans (see chapter 
14) do not post it 
yourself. Take it to 
the state pathology 

Preparing the Specimen 

Your goal is to find abnormalities such as abscesses, tumors, inflamma- 
tion, fluid accumulation, foreign materials, changes in muscle or bone 
condition, and irregularity in the size, shape, or color of internal organs. Exam- 
ine not just dead birds but at 

least one bird that recently be- 
gan showing symptoms and one 
in which the disease is quite far 

Examining birds in various 
stages of illness shows how this 
particular disease progresses, 
which may help you determine 
what the disease might be. 
Checking more than one bird 
also helps you determine which 
signs are specific to individuals 
(therefore possibly insignificant) 
and which are flock-wide occur- 
rences (likely signs of disease). 

Kill a bird for posting by stretching its neck. When a bird is not already 

Postmortem Examination 169 

dead, you will have to kill ii. If that sounds like a drastic measure, remember 
you're doing it out of concern for the rest of your chickens. If a serious illness is 
gripping your Hock, this and other birds may die anyway. Your goal is to deter- 
mine the cause so you can prevent additional deaths. 

The best way to kill a chicken for posting is to stretch its neck, which pain- 
lessly breaks the neck and spinal cord. With one hand, hold the bird's feet. 
Grasp the bird's head with the other hand, your thumb behind its comb and 
your little finger beneath its beak. Tilt the head back and pull steadily until the 
head is separated from the neck. 

Continue to hold the head up until the bird stops struggling. Otherwise, it 
may spit up and inhale crop contents, leaving the false impression that the 
disease caused the respiratory system to fill with foreign matter. 

Wait a few minutes while blood collects and clots beneath the neck skin, 
and the body tissues firm up. Meantime, examine external openings and run 
your hands over feathered areas to find lumps or odier irregularities. 

Position of in tenia I organs - Horizontal 

170 Tin; Chicken Health Handbook 

Conduct your postmortem outdoors or in a garage or carport, using a table 
or the tailgate of a pickup truck as your work surface. (Posting a diseased bird 
in a kitchen where food is prepared is not a sensible idea.) Cover your work 
surface with clean paper. Wear rubber gloves and an apron. 

Use water and detergent in a spray bottle, or a wet cloth, to dampen the 
bird's feathers so they won't blow around. Lay the bird on its back. Holding 
one leg away from the body, cut the skin between the leg and the abdomen. Do 
the same on the other leg. 

Stabilize the bird by bending the legs back, one at a time, until die joints 
snap to let the legs lay flat against the table. Cut the skin from the vent to the 
throat. Note any bloody spots or streaks in the breast or thigh muscles. 

Position of internal organs - Vertical 

Postmortem Examination 171 

Use scissors to cut through the abdominal wall just behind the point of the keel. 

About halfway from the vent to the keel, cut through the abdomen wall 
crosswise from one leg joint to the other. Use a pair of heavy scissors, kitchen 
shears, or tin snips to cut upward on one side, through the rib cage and other 
bones, taking care not to cut into or disturb the internal organs. Stop cutting 
just short of the wing joint. Make a similar cut on the other side, only this time 
cut all the way through the wing joint. Note how easy or difficult it is to cut the 
bones — an indication of their condition. 

Lift the breast and rotate it on the uncut joint as if it were a hinged cover. 
Now you can see the internal organs in their natural position. 

Examining the Organs 

Take hold of the gizzard in the palm of one hand, your thumb and forefin- 
ger grasping the stomach (proventriculus), and make a cut between the 
stomach and the crop. With one hand, lift the stomach away. With the other 
hand, loosen and remove the gizzard, liver, spleen, and intestine. Set them 

172 The Chicken Health Handbook 

Carefully separate the 
gizzard from the stomach 

aside, leaving the intestine attached to the vent. Examine the heart, lungs, re- 
productive organs, kidneys, and nerves still in place. 

To examine the contents of the digestive system, use your shears to cut 
longways through the stomach, gizzard, intestine, and ceca. Note any para- 
sites present. Also note any unusual odor, especially related to the crop or 

To examine the respiratory system, cut through the corner of die mouth 

^£ Examine the digestive system 
by cutting longivays through 
the stomach, gizzard, 
intestine, and ceca. 

Postmortem Examination 173 

Digestive tract infected with large roundworms (Ascaridia galli) 

and expose Ihe throat and crop. Then cut down the windpipe from the back of 
the mouth to the lungs. 

To examine the head, cut across the face, half-way between the nostrils 
and the eye. Note any unusual odor coming from the nose area. 

If the bird was lame or paralyzed, cut through the ligaments of one hock 
joint and twist the leg until the joint pops open. Break the leg bone, both to 
examine the marrow cavity and to test the bone's strength. A healthy bone 
makes a snapping sound when it breaks. 


Without using a microscope and staining techniques to examine tissue, 
you will not be able to observe minute changes caused by illness. There are, 
however, plenty of obvious changes to look for. 

In technical terminology, easily observable changes are called "gross le- 
sions" ("gross" meaning large and "lesion" being medical jargon for 
alteration). A gross lesion is any visible change in the color, size, shape, or 
structure of an organ. Examples of lesions are: tumors, inflammations, accu- 
mulations of fluid, dead tissue, and enlarged organs. 

Pay attention to: 

• the location of the lesion (note specific organs) 

• the nature of the lesion (its size, shape, color, and consistency) 

• the possibility that the lesion killed the bird (by blocking airways or 
intestines, through extensive bleeding, by destroying a vital organ, by 
causing paralysis) 

1 74 The Chicken Health Handbook 

Try (o determine the possible cause of the lesion — infection, nutritional 
deficiency, poisoning, injury, or whatever. Determining the cause often re- 
quires microscopic analysis, but some causes are fairly obvious, such as 
worms or injury due to cannibalism. 

Lesions, like symptoms, may be general or specific. A general lesion can be 
caused by any of several diseases. A specific lesion is characteristic of a particu- 

Postmortem Findings 

Body Part Finding Age/Sex Possible Cause 


fragile, thin, soft 


cage fatigue 

soft, rubbery 







tumors in marrow 

2 years 



fatty marrow 


lymphoid leukosis 


infectious anemia 


brnkfn vn\k 

111 lHeK 

I *\ 1 ■ i Mi'nm \~i r~\i r\ lori 
LHUILUIJIU, I 1 M Ml 111, 


colibacillosis. infectious 

bronchitis, pullorum 

rlrifwl nut 

tineu OUT 


infectious bursal disease 

vm i no 

1 1 If ft ci I ! \ip prifjintic 
UIL.C1 till VL t-IlldlLla 


ft mil 1 \'i ivori 1 1 

2 years 


UIOOU spoucti 




white streaks 


white muscle disease 

Willi' 1 ' I 1 i '- 1 I 





arizonosis, blackhead. 

coccidiosis, salmonellosis 




yellow nodules 


ulcerative enteritis 

yellowish, watery 




rotaviral enteritis 


swollen, cheesy 


infectious bursal disease 




infectious anemia 


runting syndrome 



lymphoid leukosis 


empty or foul fluid 








crop impaction 




sticky mucus 



Turkish-towel look 



Postmortem Examination 175 

Body Part Finding 

Age/Sex Possible Cause 

Heart film covered 

pale, yellowish 
pale, enlarged 

yellow, enlarged 
spotted, enlarged 
enlarged right side 
surrounded with fluid 
Intestine mucus tilled 

greenish mucus 
watery mucus 
sticky mucus 
bloody mucus 

foul brown fluid 
yellowish buttons 
yellowish, watery 
inflamed, slimy 


pale, distended 

yellow or gray knobs 

Kidneys grayish dots 
spotted, pale 

swollen, spotted 

swollen, dark 
swollen, pale 

young air-sac disease 

all chronic respiratory disease 

chicks arizonosis 

all fatty liver syndrome 

young listeriosis 

mature streptococcosis 

all spirochetosis 

growing round heart disease 

chicks pullorum 

growing broiler ascites 

all cholera 

all lymphoid leukosis 

young infectious bursal disease 

pullets bluecomb 

all ochraioxicosis 

all spirochetosis 

all campylobacteriosis 

mature cholera 

all colibacillosis 

chicks coccidiosis 

all leucocytozoonosis 

young necrotic enteritis 

young ulcerative enteritis 

young rotaviral enteritis 

all typhoid 

all ergotism 

all paratyphoid 

chicks coccidiosis 

all pullorum 

young infectious stunting syndrome 

young sudden death syndrome 

2 years tuberculosis 

all colibacillosis 

growing infectious synovitis 

chicks salmonellosis 

mature lymphoid leukosis 

all paratyphoid, 

typhoid, erysipelas 

growing Marek's disease 

all pseudomonas 

pullets bluecomb 

chicks infectious bursal disease 

all goul (visceral), infectious 

bronchitis, ochractoxicosis. 


(chart continues, oner) 

176 Tiii; Chicken Health Handbook 

Body Part 


Postmortem Findings (cont.) 

Finding Age/Sex Possible Cause 



infectious anemia 



lymphoid leukosis 

shriveled or enlarged 


gout (visceral) 



air-sac disease, chronic 

respiratory disease 



necrotic dermatitis 


lymphoid leukosis 

swollen, mottled, yellow 


algae poisoning, erysipelas 



swollen, discolored 


broiler ascites 



swollen, gray spots 



swollen, gray areas 


Marek's disease 

swollen, bronze or green 



swollen, greenish 


infectious synovitis 

swollen, red 



swollen, red streaks/white dots 



swollen, white or gray nodules 


swollen, spotted 




ochratoxicosis, pseudo- 

monas, spirochetosis 



infectious anemia, blackhead, 


patchy red or pale 



mot tled with yellow 


ulcerative enteritis 




mushy, yellow 


fatty liver syndrome 







greenish with red spots 


infectious anemia 

yellow "stars" 



needle-like crystals 


gout (visceral) 



Marek's disease 


lymphoid leukosis 

gray or yellow nodules 

2 years 


green, furry balls 






grayish yellow 



yellow "pearls" 






red, bloated 


sudden death syndrome 





broiler ascites 

mature cholera 

Postmortem Examination 177 

tsociy Iftn i 


Age/ sex 

rOSSluie L.UIIS6 


white or gray nodules 






lymphoid leukosis 



Marek's disease 


gray or white nodules 

2 years 


gray white tumors 


Marek's disease 





erysipelas, leucocytozoonosis 

swollen, red 



swollen, dark, soft 



swollen, spotted 


ulcerative enterids, infectious 

bursal disease 





■^wnllpn nfllrhv 



Marek's diseasp snirochptosis 






infectious anemia 



lymphoid leukosis 

gray or yellow nodules 

2 years 



gray white tumors 


Marek's disease 

swollen, bloody 


infectious stunting syndrome 




infectious bronchitis, 

gout (visceral) 

lar disease. Few lesions are specific; most are general, testing your power of 

Sometimes you can identify a disease by the organ on which a lesion oc- 
curs. Other times you might identify a disease by the combination of lesions 
you find. When more than one disease is involved, as is often the case, the 
combination of lesions they produce can be confusing. 

Asastardngplace, look up any lesion you find in the charts in this chapter. 
Then look up the indicated disease in the alphabetic list in chapter 15 to see if 
the overall description of that disease matches the condition of your birds. 


Each time you post a chicken, write down your findings in your flock his- 
tory, even if you aren't sure what disease the bird might have. The information 
may become helpful later on, especially if a serious disease is progressing 
through your flock. 

Veterinarian Arthur A. Bickford, a poultry pathologist in California, sug- 
gests that you not worry about trying to use proper technical jargon. Just write 

178 Thk Chicken Hi-alth Handbook 

down what you see. If you're not sure what you're looking at, but you know 
something isn't right, jot down the location and describe it as "abnormal." If 
you don't know whether you're looking at a tumor or an abscess, write "lump." 
Getting too specific when you're not sure may cause confusion if you later sub- 
mit your notes to a diagnostic lab. 

Tissue Samples 

If you find similar lesions in several birds, you might send tissue samples to 
die path lab for examination. Sending samples is particularly handy if the lab is 

the pathologist will need. 

To make a tissue sample of the organ involved, take a slice at least Yt inch 
(1 cm) thick. Include healthy-looking tissue as well as abnormal tissue. Place 
the sample in a clean, unbreakable container and cover die sample with 10 
percent formaldehyde solution. (If you can't get formaldehyde from your 
druggist or veterinarian, you might get a little from a local high school or col- 
lege biology lab or from a funeral home. Call first, and bring your own 
container — these sources are not in the business of distributing formaldehyde.) 

Be sure the container holding the sample is sealed well so it won't leak. 
Pack it in a carton surrounded by plastic peanuts or an ample amount of other 
packing material. Include the same detailed history of die disease you would 
prepare if you were submitting whole birds. 


An inflammation or swelling is only one kind of lesion, but the most com- 
mon one. Inflamed conditions are identified by the suffix "itis" following die 
technical name for the body part that's inflamed. If it all sounds like Greek to 
you, that's because it is — the medical terms for various body parts are derived 
from the Greek language. 

Words ending in "itis" are not necessarily diseases, but are often caused by 
several different diseases. It's helpful to know the names of the various "itises" 

in a technical poultry manual. (See next page for a list of inflamed conditions.) 

Diagnosing Nutritional Deficiencies 

Like infectious diseases, nutritional deficiencies may cause gross lesions 
that, together with otiier symptoms, can be used to identify the cause. Since 
nutritional deficiencies are no longer common, their characteristic lesions are 

Postmortem Examination 179 

listed separately here, along with additional symptoms as a diagnostic aid. 
For a fuller description of nutritional problems, see the section on nutritional 
diseases in chapter 2. 

Chart 10-2 

Inflamed Conditions 

Condition Body Part 

Common Cause 

Airsacculitis air sacs 

Arthritis joints ("arthron") 

Conjunctivitis eye lining ("conjunctiva") 

Encephalitis brain ("enkephalos") 

Enteritis intestine ("enteron") 

Hepatitis liver ("hepatos") 

Nephritis kidney ("nephros") 

Pericarditis membrane surrounding abdominal 
organs ("peritoneum") 

Rhinitis nasal passage lining ("rhinos") 

Salpingitis oviduct ("salpinx") 

Septicemia blood ("septikos" = putrefaction; 
"hamia" = blood) 

Sinusitis sinus cavities 

Synovitus membranes lining joints 








ammonia fumes 
eye worm 



infectious anemia 

gout (visceral) 



Escherichia coli 

Escherichia coli 


Escherichia coli 

Streptobacillus moniliformis 

180 Tut CiucKtN Handbook: 

Chart 10-3 

Nutritionally Rel 

Age/Sex Finding 

lated Findings 

\< inn u >iuti oyiiifJviJiiio 

ijxzj tot (-/to y 


swollen hip nerve, 

walking on h ricks 


toes curved inward 

blue green gelatinous 

bluish breast and legs 


fluid under skin 

soft, swollen, greenish 

retracted head, prostra- 

vitamin E 

yellow brain; or bluish green 

tion, death 

fluid under skin and blood 

spots in leg and breast muscles; 

or light streaks in breast muscles 


blood spots in muscles, slow 
blood clotting, pale marrow 

pale comb, bleeding 
wattles, bleeding eye 

vitamin K 


broken yolks in body cavity 

shrunken, bluish combs, 
wattles, prominent leg 
tendons on back of legs 



swollen kidney, crystals in 

off-color droppings, 
shrunken muscles 


white sores in mouth 

watery diarrhea, sticky 

vitamin A 

and throat 

eyes and nose 

soft keel, collapsed ribs 

weak legs, soft beak 

vitamin D 

Disposing of Dead Birds 

Before you dispose of a dead bird, check local laws. Legal methods for dispos- 
ing of animal bodies vary from place to place. For public health reasons, 
depositing them in a dumpster or local landfill is illegal nearly everywhere. 

When the bodies are those of diseased birds, find a disposal method that 
prevents the spread of infectious agents or toxins. Do not bury them in a com- 
post pile — the warm, moist environment may provide perfect conditions for 
pathogens to keep multiplying, and flies and rodents may spread the disease. 

The two best disposal methods are burial and burning. Bury bodies deeply 
so they can't be dug up by dogs or wild animals. Find a spot far from wells, 
streams, and other water sources. While you're at it, bury all contaminated lit- 
ter, feed, and droppings associated with the diseased birds. 

Burning may be necessary where the water table is high, the soil is rocky or 
frozen, or burying is prohibited by law but burning is not. You'U need a heap of 
combustible materials — scrap wood or tree prunings, along widi diy straw for 
a hot blaze. Make sure the carcasses are fully burned, then buiy the ashes. 


SOME CHICKEN DISEASES CAN BE CURED if treatment starts early. Others 
are irreversible or fatal. By the time chickens show obvious signs of illness, the 
disease is usually pretty far along. Recognizing a disease as soon as it starts is 
the first step toward curing the ones that are temporary and dealing effectively 
with those that are permanent or irreversible. The longer you wait before you 
take action, the more difficult treatment or control becomes, and the more 
losses you may incur. 

Treating Sick Birds 

Attempting to treat a flock without knowing what's wrong can be costly, may 
result in continuing losses, and could make the disease worse. For example, if 
you treat chickens with a drug that's appropriate for coccidiosis when in fact 
they have infectious anemia (a disease with similar symptoms), you will make 
matters significantly worse. 

Once you identify the problem, you have three choices: 

• cull the affected birds 

• wait until the disease goes away 

• embark on a course of therapy 


182 The Chicken Handbook 

In this context, cull means kill. When a condition is serious, sometimes the 
only humane approach is to put the birds out of their misery. Some serious 
diseases should not be cured because recovered birds will be carriers, continu- 
ing to spread disease intermittendy or continuously, for die rest of their lives. 
Other diseases are so contagious that the only way to keep them from spread- 
ing is to destroy the diseased flock. 

If you are raising chickens to get healthful meat, you may prefer to cull 
diseased birds and start over, radier than inn die riskof eating meat containing 
drug residue or disease-causing microbes — some of which can harm hu- 
mans. By contrast, a commercial producer tries to bring as many birds as 
possible to market with a minimum of downgraded or condemned carcasses. 

If you're raising an endangered or exhibition breed, you'll likely wish to 
preserve the gene pool by keeping breeders going until you can hatch enough 

not spread through hatching eggs. You must, of course, raise die new chicks 
away from diseased adults, cull die diseased breeder flock as soon as possible, 
and meticulously clean up their housing with an appropriate disinfectant. 

Waiting until the problem goes away works only if the disease is self- 
limiting, meaning it naturally runs its course in a short time and birds recover 
on their own. Few diseases fall into that category. A good number of diseases 

treated with drugs. 

Drug Use 

Many non-prescription drugs are available from farm and feed stores and 
through mail-order catalogs. Such over- die- counter drugs are considered safe 
when they are used according to directions on the label. Whether you obtain a 
drug over the counter or by a veterinarian's prescription, it will be effective 
only if you have selected the right drug for the disease and know when to use it, 
how to use it, how often to use it, and how much to use. In addition: 

• Avoid out-of-date drugs. 

• Store drugs at 35 to 55°F (1.5-12.5°C), away from sunlight. 

• Administer a drug only as directed — If it's supposed to be given by 
mouth, for example, it may be toxic as an injection. 

• Observe the safe dosage level — The drug won't be effective in an 
amount less than the label specifies, and may be toxic in greater 

• Observe the withdrawal time when treating meat birds or laying hens. 

• Do not combine drugs or use more than one at a time, unless such a 
combination is approved by a veterinarian. 

Therapy 183 

Administering Drugs 

For a drug to be effective, it must reach the infectious microbes in suffi- 
cient quantity and remain in contact long enough to do the job. Most drugs 
should be administered for at least 3 days, or for 2 days after the symptoms 
disappear, whichever is longest. As a general rule, if you do not see some im- 
provement within 2 days, you are using the wrong drug. 

How you administer a drug depends on the drug you use, the disease 
you're treating, the number of birds involved, their condition, and the length 
of time the drug must be administered. Drugs can be applied: 

• topically 

• orally 

• by inhalation 

• by injection 

Topical or local medications are applied directly to the skin, eyes, nose, or 
other external organs. Examples of topical drugs are antibiotic powders or 
ointments used to prevent infection of wounds, and liquids applied to an in- 
fected eye. 

Oral medications are given by mouth. They work either by controlling mi- 
crobes in the intestine or by being absorbed 
through the intestine to be distributed to other 
parts of the body. Oral drugs take effect slowly, 
usually in 4 to 12 hours, depending on the drug 
used, the bird's metabolic rate, and the amount 
of feed in its crop. Oral drugs are convenient and 
safe, but can be unpredictable in their absorption 
rates, especially when a bird has diarrhea. Ex- 
amples of oral medications are tablets, capsules, 
feed or water additives, and drenches. 

Inhaled medications work against microbes 
in the respiratory system or are absorbed through 
the respiratory system to be carried to other parts 
of the body. Such a drug may be a liquid solution 
applied by means of a fine mist or a dust puffed 
into the air. Specialized equipment is needed to 
put particles of just the right size and density into the air, making the use of 
inhaled drugs impractical for small flocks. 

Injected medications, which take effect rapidly, are inserted with a needle 
and syringe into one of three places: beneath the skin, into the muscle, or into 
the bloodstream. 

Shots, tablets, and drenches are suitable for treating individual chickens. 

A liquid medication, 
or "drench," is in- 
serted i nto a chicken 's 
mouth by means of a 
syringe fitted with a 
short piece of plastic 
tubing that lets you 
squirt the liquid into 
thebird's throat — tak- 
ing care not to get any 

They ensure that each bird gets an adequate dose, but administering them is 
time-consuming and handling each bird can increase stress and aggravate the 

Drugs administered by feed, water, or through the air are suitable where a 
large number of birds are involved or the drug must be administered over a 
long period of time. Although flock administration saves time, you can never 
be sure each bird gets an adequate dose. 

Feed and Water Additives 

When medications are added to feed or water, low birds in the peck order 
may not spend enough time at the trough to obtain a sufficient dose. Further- 
more, there's always the danger that birds won't eat or drink at all, or will eat or 
drink to excess and overdose. 

If a medication must be administered by means of feed or water, adding it 
to water is preferable for two reasons: 

• many diseases cause appetite loss and increased thirst; 

• on a small scale, diluting a drug in water is easier than trying to stir it 
evenly into feed. 

Some small-scale flock owners medicate feed or drinking water either rou- 
tinely or during times of stress as a precaution against disease. The practice is 
not only expensive but counterproductive, since it has little or no effect in pre- 
venting disease, and can cause resistant strains of microbes to develop so that 
drugs won't work if a disease does strike. 

Commercial growers add low levels of drugs to rations to improve eggpro- 

Diluting Medications 

When a drug label calls for medicating feed at a level of 200 parts per million 

(ppm), an equivalent amount in drinkin 

g water would be 400 milligrams per 

gallon (assuming chickens consume twice as much water as feed). 

When instructions call for diluting a 

drug 1:2000 in water, combine: 


with water 

2 tablespoons (1 ounce) 

16 gallons 

1 tablespoon C/2 ounce) 

8 gallons 

V2 tablespoon* ('A ounce) 

4 gallons 

1 teaspoon 

2'/ 2 gallons 

Vz teaspoon 

5 quarts 

"You can find a <A tablespoon measure with ih 

> canning and freezing supplies at most 

discount department stores. An equivalent measure is l'/z teaspoons. 

Therapy 185 

duction and to stimuJate the growth rate and feed-conversion efficiency of 
broilers. For unknown reasons, antibiotics cause a bird's intestinal wall to thin, 
improving nutrient absorption. But the routine non-medicinal use of antibiotics 
in food-producing flocks leads to antibiotic resistance in humans as well as in 
the chickens (see "Antibiotic Residues," page 191). 


Whenever you administer a drug by injection, use a fresh or sterile needle 
and syringe. To sterilize a used needle and syringe, separate them, boil them in 
clean water for 1 5 minutes, dry them on a clean paper towel, and store them in 
a clean, dust-free place. 

If you use the same needle to inject more than one bird, before refilling the 
syringe between birds, dip the needle in alcohol (unless you are applying a 
live-virus vaccine), or pass the needle through a match flame. Keep extra 
needles on hand in case the one you're using gets too dull to pierce easily. 

Use a 20-gauge needle, 3 A inch (.75 cm) long for chicks, 2-inches (5 cm) 
long for mature birds. Syringes are marked off in cubic centimeters (cc) and 
portions thereof. Drug dosages are specified either in ccs or in ccs per pound of 
weight. To determine how many ccs you need, multiply the bird's weight by 
the number of ccs per pound. Sometimes dosages are given in milliliters (ml). 
Since 1 ml equals 1.000027 cc, for practical purposes they are the same. Use a 
syringe large enough to hold the entire dose in one shot. 

Subcutaneous injections (SC or SQ) are given directly under the skin, usu- 
ally at the breast or the nape of the neck where the skin is loose. Pick up a pinch 
of skin and insert the needle at an angle. If you're injecting chicks, take care not 
to push the needle all the way through the skin 
and squirt the drug out the other side (or into 
your thumb). A subcutaneous injection is easy 
and safe to administer and lasts a long time — 
up to 2 days. On the other hand, the drug takes 
effect slowly because it requires a long time to 
migrate to the bloodstream for distribution 
throughout the body. 

Intramuscular injections (IM) go into the 
meaty portion of the breast. They take effect 
fast — in about an hour — and last about 8 
hours, but you must take care not to touch a 
bone or nerve, or deposit the drug into fat or the 
bloodstream. Insert the needle straight into the 
breast muscle, at a right angle. Before injecting 
the drug, pull back on the plunger. If blood ap- 


186 The Chicken Health Handbook 

pears in the syringe, move the needle to another spot. Otherwise, yon may kill 
the bird by inserting the drug directly into its bloodstream. 

Intravenous injections (IV) insert medication directly into die bloodstream, 
where it takes effect almost immediately. They are the trickiest shots to give 
and should be used only for drugs designed for IV administration, and only on 
a bird that's comatose, paralyzed, or otherwise in imminent danger of dying — 
IV administration of C. botulinum antitoxin, for example, might be used on a 
valuable breeder that 's been paralyzed by botulism. 

An fV injection goes into die main wing vein or brachial (see the box on 
page 149). First, pull a few feathers from the depression in the upper part of the 
underside of one wing, so you can better see the main vein. Insert the needle 
into die vein, pointed toward the wing tip (away from the chicken's body) and 
depress the plunger to release the drug very slowly. 


All drugs derived from fungi or bacteria and used against other living organ- 
isms are called antibiotics (and meaning against and biotic referring to living 
organisms), or sometimes antimicrobials. The use of antibiotics and other 
chemicals is controlled by the FDA (Food and Drug Administration), USDA 
(United States Department of Agriculture), and EPA (Environmental Protec- 
tion Agency). With all these agencies involved, it's not surprising that 
regulations change constantly. If you want to know the current status of any 
drug to be used on chickens, consult the Code of Federal Regulations, The Fed- 
eral Register, and die Feed Additives Compendium (all listed in the appendix). 
Antibiotics fall into six basic categories: 

• anthelmintic — against worms (discussed in chapter 5) 

• anti-protozoal — against protozoa (see chapter 6) 

• antiviral — against viruses 

• anti-fungal — against mold and fungi 

• antibacterial — against bacteria 

Antiviral Agents 

Viruses are difficult to treat with drugs, and to date no safe, broad-spec- 
trum antiviral drug has been discovered. A virus in the environment neither 
eats nor breathes, and is therefore impervious. Once a virus attaches itself to a 
cell in a chicken's body, any drug that harms the virus tends also to harm the 
infected cell. Treatment of viral diseases largely involves alleviating symptoms 
(in a respiratory infection, for example, using a product such as Vicks or VetRx 

Therapy 187 

while its immune system fights the virus. 

Antiviral drugs may soon become available that either keep viruses from 
invading cells or interfere with their replication within a cell. The most promis- 
ing of these is interferon. When a virus attacks a cell, the cell produces the 
natural protein, interferon, that keeps the virus from multiplying and infecting 
additional cells. The problem is that insufficient amounts of interferon are 
within the body produced to stop an especially virulent virus. 

Interferon can be artificially produced and has successfully been used in 
massive doses to treat a variety of viral diseases, including influenza and 
Newcastie. It may also be combined with vaccines to provide temporary pro- 
tection while immunity is developing. Interferon may soon become less 
expensive and more readily available. 

Anti-fungal Agents 

Fungal diseases, like viral diseases, do not respond well to drug treatment. 
Not only are fungi somewhat impervious to drugs, but drugs interfere with a 
chicken's nauiral microflora, making room for fungi to run rampant — the rea- 
son fungal infections commonly follow the use of antibiotics in treating other 

Copper sulfate (CuSO,), also known as "powdered bluestone," is toxic to 
fungi and can be used to prevent or control many fungal diseases. Clean feed- 
ers, waterers, and other equipment with an 0.5 percent solution. Treat birds 
widi a 1:2000 concentration in drinking water (V2 teaspoon per gallon) every 
other day for a week. Take care — a concentration of 1 :500 or greater is toxic to 
chickens. Due to the possibility of a chemical reaction between copper sulfate 
and galvanized metal, do not use a metal waterer. 

amphotericin B (trade name Fungizone), gentian violet, iodine, and nystatin 
(trade name Mycostatin, among others). Any drug used to treat a fungal infec- 
tion (ringworm, athlete's foot, etc.) of pets or humans can be tried on a 
chicken. You can't tell in advance what will work, since fungi are resistant to 
many drugs. Furthermore successful treatment requires persistence, since a 
chicken with a superficial fungal disease infects other birds and reinfects itself. 


Most antibiotics are antibacterials, and some antibacterials work against 
fungi and protozoa as well as bacteria, so the two words are often considered 
synonymous. A narrow-spectrum antibacterial is effective against a specific 
bacteria or group of bacteria. A broad-spectrum antibacterial is effective 
against numerous kinds. 

1 88 The Chicken Health Handbook 

Whether an antibacterial is narrow-spectrum or broad-spectrum, its ef- 
fectiveness will be reduced in a bird diat has been infected for a long time or 
whose immunity has been weakened due to poor sanitation, malnutrition, or 
the presence of a viral infection. Although antibacterials have no effect against 
viruses, they are often used in treating viral diseases to keep weakened birds 
from getting a secondary bacteria] infection. 

Antibacterials that destroy bacteria are called "bactericidal." Antibacteri- 
als that retard the growth of bacteria, thereby giving the immune system time 
to produce antibodies and otherwise rally its own defenses, are called "bacte- 

Sulfonamides or sulfa drugs were introduced in the 1 93()s as the first medi- 
cations used to treat infection. Originally they were effective against a wide 
range of bacteria. Many bacteria have since become resistant, particularly sta- 
phylococci, Clostridia, and pseudomonas. Nevertheless, sulfa drugs are still 
used today because of their low cost relative to their effectiveness. They should 
not, however, be used to treat laying hens. 

The sulfonamide group includes several related drugs, easily identified 
because their names almost always start with "sulfa." They fall into two cat- 

• rapidly absorbed and rapidly excreted, requiring treatment one to four 
times a day; 

• rapidly absorbed and slowly excreted, allowing treatment only once 
every second or third day. 

Most sulfonamides are bacteriostatic, but some can be bactericidal, de- 
pending on the dnig, the dose, and the bacteria involved. Sometimes three 
different sulfonamides are combined to create a more effective tablet or liquid 
medication called "triple sulfa." 

Sulfa drugs are added to drinking water for the treatment of bumblefoot, 
toxoplasmosis, a variety of respiratory infections, systemic colibacillosis (often 
in combination with penicillin G), and coccidiosis (see "Drugs Used to Treat 
Coccidiosis," page 103). The sulfas work best when treatment starts in the early 
stages of infection. A chicken usually shows improvement within 3 days, but 
should be treated for an additional 2 days after symptoms disappear. 

In any case, sulfa treatment should not go on longer than 7 days or the 
result may be kidney damage and/or vitamin K deficiency (interfering with 
blood clotting), hi addition, if a chicken does not drink enough water during 
treatment, its pH balance becomes too acidic. If prolonged treaunent is neces- 
sary, add 1 tablespoon of sodium bicarbonate (baking soda) per gallon to the 
drinking water. 

The penicillins are a large group of antibiotics derived from mold and 
identified by names ending in "cillin." The first penicillin was discovered in 

Therapy 189 

1 928 by a bacteriologist named Fleming who wanted to know why bacteria do 
not grow in die presence of mold. When penicillin was first used in 1941 , it was 
considered a miracle drug and was administered so indiscriminately that 
many strains of bacteria have become resistant. 

The penicillins may be bactericidal or bacteriostatic — depending on the 
sensitivity or resistance of the bacteria involved — and are used to treat a vari- 
ety of acute infections. They fall into two types: 

• Natural penicillin (such as penicillin G) works against a narrow spec- 
trum of bacteria, including some strains of staphylococci, streptococci, 
and E. coli. It is sensitive to light and heat, so is usually mixed just 
before it is used. Natural penicillin is poorly absorbed by the intestine, 
and so must be administered by intramuscular injection. 

• Semi -synthetic derivarives (such as ampicillin and amoxicillin) absorb 
better than natural penicillins and can be given orally. They work 
against a broader spectrum of bacteria that have become resistant to 
natural penicillins, including most strains of E. coli and Salmonella. 

in "cycline." There are three naturally occurring tetracyclines and a number of 
their derivatives, all bacteriostatic against the same kinds of microbe — some 
chlamydia, staphylococci, streptococci, mycoplasmas, and a few other groups 
(but not most strains off. coli). 

The tetracycline most often used for chickens is oxytetracycline (trade 
name Terramycin), which comes both in injectable form and in a powder to be 
added to drinking water. Since it works best in an acidic environment, its ab- 
sorption rate can be improved by adding 1 cup of cranberry juice, Vz cup of 
vinegar, or 2 teaspoons of citric acid (from the canning department of a gro- 
cery store) to each gallon of drinking water. To further increase the drug's 
effectiveness, discontinue calcium supplements during treatment. Despite 
the broad spectrum of tetracyclines, Uiey work rather poorly and are used in 
industry primarily as growth promoters. 

Aminoglycosides get tiieir name from the fact that each contains at least 
one sugar (glycoside) attached to one or more amino groups. They kill bacteria 
diat multiply rapidly — such as those causing enteric and septicemic diseases 
— after only brief contact, but die drugs have no lasting effect. The group includes: 

• Gentamicin (trade name Garasol), a very broad spectrum antibacterial 
administered as an intramuscular or subcutaneous injection to treat 
systemic infections, particularly those caused by £ coli. 

• Neomycin, used for staphylococcal skin infections such as bumblefoot 
and infected breast blister. As a topical antibiotic, neomycin comes in 
powder form (trade name Neo-Predef) or as an ointment (trade name 

190 The Chicken Health Handbook 

Neosporin, among others). Neomycin sulfate is used orally to treat 
diarrhea caused by susceptible /;'. coli and Salmonella. 
• Streptomycin, given as an intramuscular or subcutaneous injection, 
works against a fairly narrow range of susceptible E. coli, Pasteurella, 
Salmonella, and staphylococci. 

Aminoglycosides are often combined with penicillin to create synergism 
— a phenomenon whereby two drugs applied together have a greater total ef- 
fect than the sum of their individual effects. An example of a synergistic 
combination is penicillin and streptomycin (trade name Combiotic, among 

Erythromycin (trade name Gallimycin) belongs to a group of broad- 
spectrum drugs called "macrolides". It is so similar to penicillin that it is often 
considered an alternative. It is basically a bacteriostat, but in large doses can be 
bacteriocidal. Erythromycin is used to treat superficial staphylococcal and 
streptococcal infections, as well as chlamydiosis, mycoplasmosis, and 
salmonellosis. It is usually given orally, but absorption is poor unless the stom- 
ach is empty. An intramuscular injection absorbs more rapidly, but causes 
swelling and pain. 

Bacitracin (trade name Solu-tracin 50) is similar in range to penicillin G, 
but does not absorb well in the intestine and is relatively toxic when given as an 
injection. It is mainly used topically to treat staphylococcal and streptococcal 
infections of the skin and mucous membranes. (It is also used in industry as a 
growth promoter.) Besides being bacteriocidal, bacitracin is also both 
fungistatic and fungicidal. Combined with neomycin, it's sold as the antibac- 
terial ointment, Neosporin. 

Antibiotic Reactions 

Antibiotics can cause reactions that are as bad as, or worse than, the dis- 
ease they're used to treat. For starters, they upset the balance of normal 
microflora in a chicken's body, particularly in its digestive tract, paving the way 
for entry by additional disease-causing bacteria and fungi. A classic symptom 
is diarrhea, which can be fatal if the drug is not discontinued. 

Long-term use of sulfa drugs can cause vitamin K deficiency due to inhibi- 
tion of the microflora that normally synthesize this important vitamin 
responsible for normal blood clotting. Infectious anemia may result unless the 

Anaphylactic shock, a violent allergic reaction, may result from repeated 
antibiotic injections. Symptoms are paleness and rapid loss of consciousness. 
Swelling within the respiratory system may cause death through asphyxiation. 

Therapy 191 

The routine use by commercial growers of low levels of antibiotics, par- 
ticularly penicillin and tetracycline, has caused more and more bacteria to 
become resistant to these drugs. The drug-resistant strains are spread through 
die use of slaughterhouse wastes as protein in rations. Since slaughterhouse 
wastes also contain antibiotic residues, feeding a flock rations that contain 
them encourages the further mutation of drug-resistant strains. 

When a diseased flock is treated with a drug, strains that are sensitive to 
that drug are destroyed, while resistant strains survive. As a result, bacterial 
diseases, particularly cholera, colibacillosis, pseudomonas, salmonellosis, and 
staphylococcosis, are becoming more difficult to treat. Successful treatment 
requires a sensitivity test to determine which drug will work against the strain 
causing the disease. 

Antibiotic Residues 

When you medicate birds raised for meat or eggs, take special care to ob- 
serve any precautions highlighted with the double Arrow Universal Warning 
Symbol. One important piece of information you'U find in the "warning" sec- 
tion of the label is the drug's withdrawal time. 

Special precautions are highlighted by this 
double Arrow Universal Warning Symbol 

in the "Warning" section of a drug label. 

body tissue and fluid, and then is gradually eliminated through the filtering 
processes of the kidneys and liver. Different drugs are eliminated at different 

The witiidrawal time on a drug label tells you the drug's elimination rate, 
or the number of days that must pass between the time you discontinue the 
drug and the time you butcher the birds for food. Remember, the withdrawal 
time is the minimum required by law — it doesn't hurt to err on the side of 
caution and add a few extra days. Before you start collecting eggs to eat, add 10 
days to any withdrawal time specified for meat birds, since substances can be 
deposited in an egg as long as 10 days before it is laid. 

Antibiotic residues in meat and eggs are harmful to humans in at least 
three ways: 

192 Ti it Chicken Health Hanuhuuk 

1. They disturb ihe natural balance of microflora in the intestines and 

2. They may cause microbes to become resistant to drugs prescribed by a 

3. They can cause a severe reaction in people who are allergic to penicillin 
or sulfa drugs. 


Jtifj food poisoning, you 

can hasten its recovery by Hushing its system with a laxative that absorbs toxins 
and removes them from the body. Although Epsom salts make the best flush, 
chickens must be handled individually, since they don't like the taste of an 
Epsom-salt solution and won't readily drink it. When a number of birds are 
involved, or handling the birds would cause undue stress, use molasses in a 
flock flush. Flush only adult birds, never chicks. 

Epsom-salt flush: 1 teaspoon Epsom salts (magnesium sulfate) in V2 cup 
water, poured or squirted down the bird's throat twice daily for 2 or 3 days, or 
until the bird recovers. 

Malmses flush: 1 pint molasses per 5 gallons water, given far no longer 
than 8 hours. 

Supportive Therapy 

Any time you treat diseased birds, isolate them away from the rest of the flock. 
After they have been moved, avoid moving diem again to minimize stress. 
When you tend your flock, take care of healthy birds first, so you won't spread 
disease from the sick ones to the healthy ones. 

Be sure the sick birds get plenty of clean water and fresh feed. Since many 
diseases cause a chicken to eat less, feed often to stimulate appetites. If neces- 
sary, move feed and water troughs so they'll be easier for the birds to reach. 
Increase die number of waterers so the birds won't run out of water during the 
day, and so those crowded around a waterer won't discourage others from 
drinking. Encourage drinking by providing cool water in summer and warm 
water in winter. 

Provide good ventilation so the chickens won't keep breathing die same- 
stale air, but avoid cold drafts that cause chilling. In cool weather, supply addi- 
tional heat, especially if the birds are young. Pay special attention to sanitation 
so the population of pathogens can't build up and reduce the birds' resistance 

water, and make sure litter is deep and clean. 

Therapy 193 

Vitamin Therapy 

Boost a flock's ability to light disease, and minimize the chance of a sec- 
ondary infection, by adding a vitamin supplement to the drinking water. A 
vitamin supplement can also be used to guard against disease in times of 
stress, such as during a move, before and after a show, during breeding season, 
or when the weather is particularly unpleasant. Chicks will get a healthy start if 
you treat them to a vitamin supplement throughout their first 3 weeks of life. 


Dehydration caused by diarrhea, worms, and other conditions depletes 
body fluids of certain minerals known as "electrolytes." They are called elec- 
trolytes because, when dissolved in water, they split into electrically charged 
particles (ions) that transmit electrical impulses. The electrolytes — calcium, 
chloride, magnesium, phosphorus, potassium, and sodium — play a vital role 
in regulating body processes and in maintaining both hydration and the 
body's acid/base balance. 

Any time a chicken has diarrhea, or otherwise suffers from dehydration, 
help its body replace and retain fluids by adding an electrolyte supplement 
e, among others) to its drinking water at the rate of 1 
Drat least a week. 

Homemade Electrolyte Solution 

If you do not have an electrolyte supplement on hand, this homemade version 
will get you through in a pinch. 


salt substitute 
baking soda 
table salt 

Va teaspoon potassium chloride 
'/2 teaspoon sodium bicarbonate 

1 teaspoon sodium chloride 

2 quarts water 

1 week, offering fresh water for the remainder of each day. 

Competitive Exclusion 

Antibiotics disrupt the microflora that normally live in a chicken's intes- 
tines and work in cooperation with the bird's immune system. To restore the 
balance of microflora following drug treatment, feed each chicken a heaping 
tablespoon of plain active-culture yogurt every day for a week. The process of 

194 The Chicken Health Handbook 

controlling beneficial microflora to help fend off disease is called "competitive 
exclusion" — the beneficial microflora provide stiff competition that excludes 

A relatively new idea in the poultry world is the use of competitive exclu- 
sion to minimize bacterial diseases by feeding newly hatched chicks the kind 
of bacteria thai naturally live in the digestive tract of an adult chicken. The ben- 
eficial immunity-enhancing microflora then have a chance to get established 
before the chicks come into contact with pathogens. You can give chicks a 
boost in the right direction by occasionally feeding them a tiny amount of 
yogurt, but take care — it doesn't take much yogurt to cause diarrhea. 

Treating Wounds 

Any injury in a poultry flock must be treated promptly, or it will attract picking 
that quickly becomes cannibalism. Wounds can be caused by faulty equip- 
ment, nails protruding from walls, serious fighting, and even mating. Cocks, 
usually of die heavier breeds, sometimes rub the protective feathers from a 
hen's back during successive matings until no feathers are left to keep the 
cock's claws from cutting through the hen's skin. 

As soon as you discover an injured bird, isolate it. Clean broken tissue from 
the wound by pouring hydrogen peroxide over it. As the hydrogen peroxide 
bubbles up. it lifts organic matter so it can be rinsed away with more hydrogen 
peroxide. If the injury is serious, remove feathers from around the edges so 
they can't stick in the wound and hinder healing. 

When the wound is clean, coat it with neomycin in the form of Neo-Predef 
powder (for an oozing wound) or Neosporin ointment (for a dry wound). If the 
injury is on the bird's foot or is quite large, wrap it in a gauze bandage and tape 
the bandage in place. To keep pus from forming and giving bacteria a place to 
grow, change the dr essing daily, clean the injury with hydrogen peroxide, and 
reapply neomycin. 

Treating Shock 

Shock is a condition brought on by a serious wound or other severe stress, such 
as an allergic reaction to antibiotics or being chased and caught by a dog and 
shaken in the dog's mouth. Shock causes pale skin, reduced circulation, rapid 
weak pulse, rapid breathing, subnormal body temperature, weakness, and 
sometimes prostration and death. If the bird is valuable enough to warrant the 
expense, and a vet is close enough at hand, the bird may recover after veteri- 
nary treatment with steroids and fluids. Otherwise, all you can do is keep the 
bird warm and calm until it either recovers or dies. 

Therapy 195 


Surgery is rarely performed on chickens, due to their relatively low economic 
value. On those rare occasions when surgery is performed, it is done to: 

• caponize broiler cocks (no longer necessary, with today's improved 
strains that grow bigger and faster on less feed); 

• decrow a valuable breeder cock (requires the services of a skilled 

• debeak birds to prevent cannibalism (see "Debeaking," page 138); 

• dub and crop fighting cocks and chickens raised in cold climates (see 
"Dubbing and Cropping," page 133); 

• clean out an impacted crop (see "Crop Impaction," page 264). 

Following surgery, treat the surgical wound as you would any other 
wound, as described above. 

What Went Wrong? 

If, despite your best efforts, sick chickens don't get better, one or more of the 
following may be the cause. 

• The diagnosis was wrong. 

■ The organism causing the disease is resistant to the drug used. 

• An inadequate dose of the drug was used. 
•The drug was; 

• The drug's expiration date has lor 

• An incompatible combination ( 

• The drug caused adverse side effects. 

• The bird was reinfected (medication was discontinued too soon). 

• An inflammation, abscess, or other condition interfered with drug action. 

• The bird has more than one infection and not all of them were treated. 

• Disease was caused by a nutritional deficiency that was not corrected. 

• The bird's defense mechanism is too low (due to the disease, drug use, or 

• Supportive therapy was inadequate. 

• Biosecurity breach was not corrected (look for ways to improve 

196 The Chicken Health Handbook 

Reportable Diseases 

Some diseases are so serious ihey must be reported either to the federal 
Animal and Plant Health Inspection Service or to your state pathology 
laboratory. Each state has its own regulations as to which diseases are 
reportable. Diseases that are designated as reportable are a serious threat 
either to the poultry industry or to public (human) health. If your flock 
experiences a sudden, high death rate (over 50 percent in a short time), you 
would do well to report it to your state veterinarian. 

If a veterinary or pathology lab diagnoses a reportable disease in 
your flock, they are bound by law to report it. The immediate result will 
be quarantine of your flock to keep the disease from spreading. In some 
cases, you may be allowed to treat your birds under strict supervision. In 
other cases, you may be required to depopulate — a polite way of saying 
your entire flock will be destroyed. If you keep chickens for commercial 
purposes, you maybe reimbursed for your loss. 

Even when your flock is not involved, if a reportable disease occurs 
in your area, the movement of all birds may be restricted. Restriction of 
movement does not occur as often with birds as it does with larger livestock, 
especially cattle, horses, and hogs. Exactly how a particular reportable 
disease is handled depends on the nature and scope of the outbreak and on 
the virulence and contagiousness of the pathogen involved. 

Reportable Diseases 

Governing Body 


Threat To 



public health 

Newcastle (exotic) 

poultry industry 

influenza (lethal form) 

public health 


public health 

(Salmonella enter; tidis) 


poultry industry 

Most states 


poultry industry 


poultry industry 

Many states 

chronic respiratory disease 

poultry industry 

infectious laryngotracheitis 

poultry industry 

'United Slates Department of Agriculture, Animal and Plant Health 
Inspection Service, Federal Building, Hyattsville, MD 20782 

Enhancing Immunity 

word for immunity is resistance; the opposite of immunity is susceptibility. A 
chick hatches with a certain amount of innate immunity and acquires new im- 
munities as it grows, but may need your help to develop additional immunity 
against diseases in its environment. 


Immunity can be broken down into two categories: 

1. Inherited — which may be: 

a. complete (all chickens are resistant) 

b. partial (some breeds, strains, or individuals are resistant) 

2. Acquired — which may be: 

a. passive, in which antibodies are transferred: 

• naturally, from hen to chick 

• artificially, by an antitoxin 

b. active, in which the production of antibodies is stimulated: 

• naturally, by disease 

• artificially, by vaccination 


Inherited Immunity 

Chickens are immune to some diseases due to inherited or genetically 
controlled factors. When the entire species is resistant, immunity is "com- 
plete." Chickens have complete immunity to a long list of diseases that infect 
other birds or animals but never infect chickens. 

As a species, chickens are immune to some pathogens they commonly 
carry in their bodies, but that make them sick if dieir resistance is broken 
down. The protozoan Histomonas meleagriclis is a classic example. It com- 
monly lives in the poultry environment, causing chickens to get blackhead 
only when their resistance is drastically reduced by a massive infestation. (Tur- 
keys, on the other hand, are highly susceptible to blackhead and often get it 
from chickens that carry the protozoa without being infected.) 

When only certain breeds, strains, or individuals are resistant to a disease, 
immunity is "partial." Chickens have partial immunity to Marek's disease, 
since some strains never succumb to the otherwise common killer. In nearly 
every disease outbreak, some individuals do not become infected due to in- 
herited immunity. Those are the birds you'll want in your breeder flock if you 
wish to breed for resistance, as described in chapter 1. 

Passive Acquired Immunity 

Acquired immunity is any resistance to disease that is not inherited, but 
instead is conferred by antibodies. Passive acquired immunity is resistance 
due to antibodies produced in die body of one bird or animal and passed on to 
the body of another. Passive immunity provides immediate but temporary re- 
sistance — since the antibodies are not produced widtin the cliicken's own 
body, immunity is short-term, lasting only about 4 weeks. 

Passive immunity may be acquired naturally or artificially. Natural passive 
immunity is acquired by a cbick from a hen via the egg. The source of maternal 
antibodies is immaterial — they may result from a disease the hen once had or 
from a vaccinadon designed specifically to build up her antibodies so she can 
pass immunity along to her chicks. 

Artificial passive immunity is acquired by a chicken when it is given an 
injection containing antibodies against toxin-producing bacteria. Botulism is 
an example of a disease caused by bacteria that produce toxins. An antibody 
that fights a toxin is called an "antitoxin." Fluid taken from the blood of an 
animal that has been immunized and therefore has antitoxins against a dis- 
ease such as botulism is also called "antitoxin." An injection of antitoxin 
confers immediate immunity, and can therefore be used to treat disease. The 
immunity is only temporary, however, since it is passively acquired. 

Enhancing Immunity 199 

Active Acquired Immunity 

Active immunity differs from passive immunity in three important ways: 

• It is caused by antibodies produced widiin a bird's own body. 

• It is not immediate but takes time, usually measured in weeks. 

• It is long-term. 

Although active immunity is always longer term than passive immunity, it 
may be temporary (as in the case of staphylococcal and streptococcal infec- 
tions), it may be permanent (as in the case of typhoid), or it maybe permanent 
unless stress weakens the bird's resistance. As a general rule, immunity to vi- 
ruses is absolute and long lasting, while immunity to bacteria is relative 
(dependent on stress avoidance) and usually temporary. 

Like passive immunity, active immunity can be acquired naturally or arti- 
ficially. Natural acquired active immunity occurs when a chicken's body 
produces antibodies to fight a particular disease (see "Immune System," page 
44). If the chicken recovers, its body continues to contain antibodies specific to 
diat disease — diey confer immunity only to diat one disease. A bird can ac- 
quire active immunity as an embryo during incubation or at any point after it 

Artificial active immunity is acquired from a vaccination containing anti- 
gens that cause a chicken's body to produce antibodies against those 
particular antigens. Active immunity resulting from vaccination takes about 2 
weeks to develop and can be renewed through one or more booster shots to 
keep the level of antibodies high enough to ward off disease. The booster dose, 
which is usually smaller than the original vaccination dose, must be adminis- 
tered at a specified time following die original vaccination. 

Acquired Immunity 







200 Tin-. Chicken Health Handbook 


itics, are used to control disease, they differ from 

• They are used to prevent rather than treat disease. 

• They do not cause resistant strains of microbes to develop. 

Since viral diseases have defied a cure, vaccines were originally developed 
to trigger immunity against viruses. Although most bacterial diseases can be 
successfully treated with antibiotics, some are so devastating that bacterial 
vaccines, called "bacterins", have aiso been developed. Few people make any 
distinction between vaccines and bacterins, but call them all "vaccines." 

Successful vaccines against some diseases have not yet been developed 
because the viruses keep changing (as in the case with influenza), too many 
different viruses cause the disease (as in infectious bronchitis), or die virus 
causing the disease hasn't yet been identified (as in infectious anemia). 

In addition, not all vaccines are created equal. Some trigger a good im- 
mune response, others confer only a low level of immunity. Some produce a 
reaction that can be as serious as the disease itself. Live virus vaccines and con- 
taminated vaccines sometimes actually transmit disease. 

ese five properties: 

; to protect chickens against infection by a 

• It contains enou; 
specific pathogen. 

• It contains antigens from all strains of die pathogen that cause the 

• It is not contaminated with additional antigens. 

• It is not too toxic to chickens (therefore causes no serious reaction). 

• It will not cause disease. 

Some state governments would like to restrict the use of vaccines to li- 
censed veterinarians and others who hold a permit. Their reasons are that 
mishandled vaccines lose effectiveness and that bootleg vaccines occasionally 
appear having little or no effect to begin with. Purchase vaccines only from 

, as evidenced by an assigned code number 

Vaccine Types 

A vaccine derived from viruses or bacteria is used to trigger a chicken's 
immune response against the viruses or bacteria from which it was derived. 
When a vaccine is administered, a chicken's body responds by producing anti- 
bodies just as it would in a natural infection by the virus or bacteria. 

Enhancing Immunity 201 

The difference between an infection and a vaccination is that die patho- 
gens in a vaccine either cause a mild case of disease or have been intentionally 
altered so they cannot cause disease at all. A chicken's antibody-producing tis- 
sue cannot tell the difference between the three basic vaccine forms: 

• live 

• modified live 

• inactivated 

Live vaccines are die most effective. They are used to induce infection, but 
to be safe they must be made from harmless microbes closely related to patho- 
genic microbes. Live vaccines are relatively inexpensive and easy to use, 
especially for mass application to large flocks, and can be applied to birds at a 
younger age than can inactivated vaccines. They cause immunity to develop 
rapidly and to spread via shedding of live viruses from successfully vaccinated 
birds to unsuccessfully vaccinated birds. 

A live vaccine has several disadvantages. It can be easily killed by heat and 
chemicals (such as alcohol used 
to sterilize a needle). It may be 
contaminated with other viruses 
during manufacture, spreading 
unintended diseases. Just as the 
virus can spread from success- 
fully to unsuccessfully vaccinated 
birds, so can it spread to suscep- 
tible nearby unvaccinated flocks. 
The vaccine produces some of the 
symptoms of the disease being 
vaccinated against and, if chick- 
ens are stressed or infected with 
some other microbe, it can cause 
serious disease. 

Because of these dangers, 
only mild viruses are used in a live 
vaccine, and multiple application is required. Live vaccines should be used 
only to prevent a serious disease already present in the yard that cannot be 
controlled any other way. Live virus vaccines are available against epidemic 
tremor, infectious bronchitis, infectious bursal disease, infectious 
laryngotracheitis, Marek's disease, Newcastle, pox, and viral arthritis. 

Modified live vaccines contain pathogenic organisms that have been ge- 
netically altered to make them less infectious so they can no longer cause 
disease, but can continue to replicate and trigger the production of antibodies. 
The process of genetically altering pathogens is called "attenuation," and 

Live Virus 

Vaccines containing live viruses are 
supposed to give birds a mild case of 
disease, but they can cause serious dis- 
ease if they are not used properly. The 
disease will remain mild if: 

• the vaccinated birds are healthy 

• they are the right age for vaccination 

• the vaccine is properly administered 

• the birds are kept warm 

• their housing is clean and dry 

• weather conditions remain steady 

202 Tin; Chicken Health Handbook 

modified live vaccines are sometimes called "attenuated" vaccines. 

A modified live vaccine is more potent than a live vaccine and is therefore 
cheaper to use, since you need less per dose. Like a live vaccine, a modified live 
vaccine must be handled carefully to avoid killing the viruses or bacteria, thus 
destroying their ability to trigger immunity. 

Like live vaccines, modified live vaccines cause shedding to unvaccinated 
birds. In addition, if attenuation is incorrectly done, the vaccine may cause 
disease rather dian immunity. Even if attenuation is correct, the vaccine 
may cause disease as a result of contamination with other pathogens or by 
interfering with the bird's immune response (making it susceptible to 
other diseases). 

Inactivated vaccines contain bacteria or viaises that have been killed by 
chemicals or heal. While most virus vaccines are live or modified live, 
bacterins are always inactivated. Inactivated vaccines are both expensive to 
produce and time-consuming to administer, since they require multiple doses 
and must be injected. Unlike other vaccines, some inactivated vaccines have a 
21 -day withdrawal lime. In addition, they may confer only short-term, low- 
level immunity. To produce a higher, more uniform response, birds are often 
primed with live vaccine first. 

On the other hand, inactivated vaccines are the easiest to store and safest 
to use. They do not cause disease in stressed or infected birds, as live and 
modified live vaccines can. They produce few adverse reactions — most com- 
monly stress due to handling and/or a lump at the site of injection, caused by 
the fluid in which the killed pathogens are suspended. 

New technologies under investigation that may one day offer terrific 
breakthroughs in disease control include biogenetically engineered recombi- 
nant DNA vaccine, for which large quantities of pure viruses can be produced 
at a relatively low cost, and synthetic vaccines that eliminate the risks inherent 
in working with genetically modified microorganisms (such as the possibility 
that genetically altered pathogens may mutate and cause new diseases). 

Vaccination Procedure 

Vaccines come in bottles containing enough for 500 or 1 ,000 birds. Even if 
you can't use it all, die cost is usually still low in relation to the cost of losing 
birds in a disease outbreak. 

Some vaccines (such as diose against Marek's disease and pox) come in 
two vials, one filled with powder and one with liquid. Once the two are mixed 
together, the vaccine is good for only about an hour, so you can't save it. De- 
stroy unused vaccine and empty containers by burning or deep burial. 

The age at which birds should be vaccinated and the precise vaccination 

Enhancing Immunity 203 

procedure you use depend on your purpose in keeping chickens and the dis- 
ease you are vaccinating against. Vaccines against some diseases come in 
more than one form and can therefore be administered by more than one 
method. Some methods of application are more suitable for flock- wide appli- 
cation involving large numbers of birds, others require handling individual 
birds to ensure that each gets an even dose. 

Water uaccinatioms die most popular 
mass method. It involves withholding 
drinking water overnight, then adding 
vaccine to the water in a measured 
amount calculated to deliver an adequate 
dose, based on die amount of water an av- 
erage bird drinks within a 3-hour period. 

feed, and weather, determine the exact 
amount of wateryour flock needs by mea- 
suring how much your birds drink the day 

A vaccine may be inactivated if the 
temperature is high or the water contains 
impurities, including sanitizers such as 
chlorine used to control bacteria or fungi. 
Do not use water sanitizers within 48 
hours of vaccinating. Clean waterers and 
rinse them well, leaving no disinfectant 
residue to inactivate die vaccine. 

The vaccine can be somewhat stabilized by adding powdered milk to die 
water. Milk protein neutralizes sanitizers and protects a vaccine from the 
shock of dilution. Before adding die vaccine, stir in skim milk powder at the 
rate of 50 grams or % cup per 5 gallons (45 g/20 liter) of cool water. (You can 
find a Vfe cup measure in the canning section of nearly any discount depart- 
ment store; an equivalent measure to % cup is 10 tablespoons.) 

Remove drinking water the night before vaccinating. Provide vaccine- 
laden water in the morning, right after mixing it. If you're treating a large flock, 
ensure that birds low in peck order get a drink by adding only half the vaccine 
to as much water as the flock will drink in about 2 hours. Then add the other 
half to as much water as die flock will drink in another 2 hours. 

tropical countries, where high water temperatures inactivate vaccines. 

Spray or aerosol vaccination offers an easy way to vaccinate large numbers 
of birds in a short time. It is most commonly used for infectious bronchitis and 

Methods of Vaccine 

Flock application 
drinking water 
feed additive 
aerosol (dust or spray) 

Individual application 
beak dip 

drop in eye (intraocular) 
drop in nose (intranasal) 
injection (intramuscular 

or subcutaneous) 
vent brush 
wing-web stab 

204 The Chicken Health Handbook 

infectious bursal vaccines, to give boosters, and to prime a flock with live vac- 
cine prior to administering an inactivated vaccine. 

Aerosol vaccination is tr icky because it can induce a severe vaccine reac- 
tion and because it requires special equipment to get the droplets just the right 
size. A fine mist penetrates deeply into the respiratory tract, a coarse spray not 
so deeply. A fine mist is used for adult birds, while a coarse spray is used to 
induce a milder reaction in chicks. 

Since birds must be confined to a small area for the aerosol method to 
work, it is most often applied in brooder housing. A hand pump may be used 
for occasional application; a coarse-spray cabinet is used by those who regu- 
larly vaccinate large numbers of chicks. 

Applying a vaccine dust by aerosol is similar, except that the powder is 
puffed dry rather than diluted and sprayed as a liquid. 

Wing-web vaccination involves the use of a two-prong stabber. The 
stabber is dipped into vaccine, then used to pierce the unfeathered skin of the 
wing-web, or the chicken's "armpit." When vaccinating cliickens of various 
ages, start with the oldest birds, then break off one prong to immunize chicks. 

The wing-web method won't work if you stab feathers instead of skin, or if 
die stabber isn't adequately immersed in vaccine. When you use a live vims 
vaccine, you can tell if the vaccinarion takes by watching for slight swelling and 
scabbing in 1 to 2 weeks. 

Injected vaccines may be administered intramuscularly (into the muscle of 
the breast) or subcutaneously (under loose skin of the breast or neck). Some 
vaccines can be applied either way. Others (such as diose against cholera and 
erysipelas) can only be administered by subcutaneous injection; a serious re- 
action will occur if they are injected into the muscle or bone. Follow 
instructions carefully as to needle size and injection site. 

Subcutaneous injection is currently the only way to administer Marek's 
vaccine to newly hatched chicks. Take a pinch of skin from the back of the 
chick's neck between your thumb and forefinger. Stick the needle into the skin 

nor stab yoi 

Eye or intraocular vaccination comes in a kit with a vial of vaccine and a 
vial of dyed mixing solution, called diluent, with an eye dropper in the cap. 
Colored diluent is used to verify proper vaccine placement in the eye — color 
appears on a bird's tongue when die procedure is correct. 

Beak dip vaccines are administered by dipping each chick's beak into the 

Vent brush vaccination requires the use of a brush to apply vaccine to the 
mucous membrane of the cloaca. This was once a standard vaccination 
method, but because it involves application of especially virulent viruses, it is 
no I 

Enhancing Immunity 205 

Chart 12-1 

Vaccination Methods* 


DE = drop in eye 

DW = drinking water 

IM = intramuscular injection 

SC = subcutaneous injection 

S = spray 

WW = wing web 


L - live vaccine 

M = modified live vaccine 

I = inactivated vaccine 










Chronic respiratory disease 





Epidemic tremor 





Infectious bronchitis 





Infectious bursal disease 




Infectious coryza 



Infectious laryngotracheitis 


Infectious synovitis 



Marek's disease 











Viral arthritis 

. I 



*Age of birds at application, method of application, and need for repeat application depends 
on the vaccine source and form — follow instructions on label. 

Vaccination Programs 

Your veterinarian or state poultry specialist can help you work out a vacci- 
nation program based on disease problems occurring in your area and your 
purpose in keeping chickens. For each vaccine you consider, take into ac- 

• its availability 

• its cost in relation to the worth of your birds 

• the size of your flock 

• your flock's expected lifespan 

• maternal immunity your chicks may inherit from your breeder flock 

• the presence of infection in your flock, your yard, and your area 

• your need for other vaccines 

• your flock's past vaccination history 

• state laws 

206 The Chicken Health Handbook 

Establish a vaccination program only to solve specific problems — past 
problems your flock has experienced or the serious threat of a new problem. 
Vaccinate against diseases your flock has a reasonable risk of getting. Do not 
vaccinate against diseases that do not endanger your flock. If you show your 
birds, if serious diseases have occurred on your place (in your own flock or in 
the previous owner's llock), or if serious diseases infect nearby flocks (particu- 
larly if you live near a high concentration of commercial chickens), you may 
have good reason to vaccinate. To learn about diseases that occur in your area, 
ask your veterinarian, county Extension agent, state poultry specialist, or the 
avian pathologist at your state diagnostic lab. In some states, it is illegal to use 
certain live virus vaccines or to introduce viruses by bringing in birds from an- 
other state that have been vaccinated with a live virus vaccine. 

Several vaccines come in combinations that trigger immunity against 
more than one disease at a time. If your vaccination plan requires the use of 
several vaccines, a combination vaccine may save you time and money. On the 
other hand, sometimes a chicken's response to one vaccine interferes with 
development of immunity to anodier. Furthermore, if your birds have an ad- 
verse reaction, you may have trouble determining which vaccine in the 
combination caused the reaction. Whenever you use a vaccine, record the 
vaccine's name, manufacturer, and serial number in your flock history. 

Vaccine Failures 

Vaccine failures usually result from improperly storing or handling a vac- 
cine or from using improper vaccinating procedures. Whenever you use a 
vaccine, read and follow instructions regarding storage and handling, method 
of application, dosage, recommended age of birds at the lime of first vaccina- 
tion, and the timing of revaccinations (boosters). All these factors affect the 
level, quality, and duration of immunity. 

If your birds are in poor health, the results of vaccinating may be worse 
than not vaccinating at all. Unless you deliberately use vaccine to slow the 
spread of pox or infectious laryngotracheilis, do not vaccinate chickens that 
have symptoms of the disease you're vaccinating against. 

Some diseases, including infectious bursal disease, reduce resistance to 
other diseases. Chicks that hatch with a good level of maternal antibodies 
against infectious bursal disease are protected against early damage to their 
immune system, but the same antibodies that confer immunity also interfere 
with the desired immune response to vaccines. 

If vaccination fails, consider these possible causes: 

• Vaccine was not stored in die refrigerator or otherwise as directed 
(improperly stored vaccines decay rapidly). 

Enhancing Immunity 207 

Vaccine's expiration date long since passed. 

Vaccine was not handled in a hygienic manner. 

Wrong vaccine was used (not all vaccines protect against all strains). 

• Vaccine was administered incorrecdy. 

• Housing sanitation is poor. 

• Flock was exposed to pathogens before immunity took effect. 

• Flock's immune response was suppressed (due to heat stress, feed 
contaminated with mycotoxins, poor health, etc.). 

No vaccine will protect your flock 100 percent — every vaccine has at least 
a 5 percent failure rate. In addition, disease can occur if you bring in new birds 
that are not on die same vaccination program as your old ones (a vaccine may 
cause your old birds or your new birds to shed pathogens). Then, too, you 
never know what disease may turn up next. Good management with an eye 
toward disease prevention remains your best defense. 

Natural Vaccination 

Before commercial vaccines became widely available, farmers practiced natu- 
ral immunization by mixing young birds with older ones, thus exposing the 
youngones to any diseases the olderones were exposed to. Genetically resistant 
flocks were developed by culling birds that did not fully recover and keeping 
(immunized) survivors as breeders. 

Chicks may be naturally vaccinated for a variety of respiratory diseases, 
most notably infectious bronchitis and mild Newcastie disease. Signs that 
natural vaccination may be occurring include mild wheezing and watery eyes. 
Cull birds that do not recover within a week so they don't have a chance to 
reproduce more weaklings. 

Other diseases for which natural vaccination commonly occurs through 
gradual exposure include chronic respiratory disease, infectious coryza, and 
infectious bursal disease. Chicks exposed to infectious bursal disease (IBD) 
before the age of 14 days rarely develop noticeable symptoms. 

Natural vaccination can backfire if chicks are exposed to massive amounts 
of microbes before immunity is complete. In at least one disease, Marek's, there 
is an alternative to gradual exposure — raise a few turkeys with your chickens. 
Turkeys carry arelated though harmless virus that keeps the Marek's virus from 
causing tumors. 

Incubation and Brooding 

start from the time they hatch. Modern practices of selective breeding and arti- 
ficial incubation have minimized some problems that occurred in the past, but 
along die way new ones have been introduced. Good hatchability and strong, 
healthy chicks result from: 

• proper egg collection and storage 

• correct operation of incubator 

• good incubator sanitation 

• healthy, well conditioned breeders 

• proper feeding of breeders 

• hereditary vigor 

Hatching Egg Care 

Collect hatching eggs several times a day so they will neither heat nor chill. To 
help you track hereditary and/or egg-transmitted problems, identify the eggs 
from each breeder or breeder group by writing a code on each egg with a 
grease pencil or China marker. If you trapnest hens to identify theireggs, check 
nests often, especially in warm weather. Hens can suffer from being enclosed 
ace, and may soil their eggs if confined in die nest too long. 

3 twenty to thirty times more bacteria on their 


Incubation and Brooding 209 

shells than eggs laid in cages. The eggs of floor-reared hens are dierefore 3 per- 
cent lower in hatchability and result in more rough red navels in newly 
hatched chicks. In addition, contaminated eggs may explode during incuba- 
tion, contaminating other eggs and causing diem to subsequendy explode. 

Bacteria on the shell, from feces or contaminated dust and nest litter, is 
more likely to get into the egg if the shell is porous. Older hens lay eggs that are 

the breeder flock, or a respiratory virus, can also cause shells to be more porous 
than otherwise. 

Manage your flock so that eggs will be clean when you collect them, which 
includes keeping litter dry so hens won't track mud into nests. Minimize bac- 
terial contamination by dry cleaning slightly soiled eggs with fine sandpaper. 
Avoid saving heavily soiled eggs for hatching. If valuable eggs become soiled 
and must be washed, use water warmer than the eggs (but not over 140"F, 
60°C), otherwise bacteria may be forced through the shell. 

Household detergent combined widi a dash of chlorine bleach (Clorox) 
serves as both sanitizer and cleaning agent. Other ways to thoroughly sanitize 
eggs: dip diem for 1 minute in a chlorine compound, quaternary ammonia 
product (such as Germex), I percent iodine solution, or other sanitizer de- 
signed specifically for use on hatching eggs. 

Store eggs in clean cartons to avoid introducing contamination during 

Egg Storage 

Hatching problems can occur due to storing eggs for too long or at the 
wrong storage temperature. The storage temperature must be below "physi- 
ological zero," the temperature above which development (however erratic) 
begins to take place. The optimum storage temperature for hatching eggs is 
55°F (13"C). The storage area should have low enough humidity not to attract 
mold, but should not be so dry diat moisture is rapidly drawn from the eggs. 

The less moisture that evaporates from eggs during storage, the greater 
their hatching rate will be. Speed of evaporation varies from one strain to an- 
other. Small eggs, such as those laid by bantams and jungle fowl, have a 
relatively large surface-to-volume ratio, so they evaporate more quickly than 
large eggs. Early season eggs of any size evaporate more slowly than late 
summer eggs. 

Eggs have a built-in ability to remain hatchable after several days of stor- 
age, otherwise a hen could not collect a batch of eggs to hatch all at one time. 
Even under the best storage conditions, hatchability drops after 6 days. You 
can increase storage time to as long as 3 weeks, while maintaining reasonable 
hatchability, by wrapping each egg in plastic wrap. 

210 The Chicken Health Handbook 


Temperature, relative humidity, ventilation, and turning during incubation all 
affect the hatch. Eggs must be turned at least three times a day at regularly 
spaced intervals, as close to 8 hours apart as possible. Fairly inexpensive incu- 
bators are available that improve the hatching rate by automatically turning 
eggs every hour. 

Ventilation is necessary to bring in oxygen and remove carbon dioxide 
generated by developing embryos. Most incubators have either adjustable 
vents you can open or plugs you can remove as die hatch progresses. 

Operating an incubator at the correct temperature can be tricky. Unless 
the incubator is extremely well insulated, temperature fluctuations in the 
room where the incubator is set up can affect the hatch. Sunlight falling on the 
incubator can cause its temperature to rise. A thermometer that isn't properly 
positioned according to die incubator manufacturer's instructions can give a 
false temperature reading. Even if the thermometer is properly placed, incuba- 
tion temperature can't be accurately set if die numbers are too close together, 
as is often die case. The thermometer itself may be inaccurate — it's always 
wise to check a new thermometer against a second or even third thermometer 
whose accuracy you are sure of. 

When incubation temperature is too low, chicks lake longer than 21 days 
to hatch. They will tend to be big and soft with unhealed navels, crooked toes, 
and thin legs. They may grow slowly or may not learn to eat and drink at all. 

When the temperature is too high, chicks hatch before 21 days. They tend 
to have splayed legs and can't properly walk, a problem that does not improve 
as the chicks grow. These chicks should be culled. 

No matter what combination of temperature and humidity is suggested by 
the manufacturer, you'll have to make minor adjustments depending on your 
location and the eggs you hatch. Keep accurate records as you make adjust- 
ments, and after a few hatches you will hit on die optimum combination for 
your pardcular situation. 

Whether your incubator is still-air (no fan) or a forced-air (has a fan), its 
optimum temperature and humidity are interrelated. As the temperature goes 
down, relative humidity must go up to maintain the same hatching rate. Here 
are some likely combinations: 

still-air: 102°F (38.9"C) at 58 percent forced-air: 99°F (37.2'C) at 56 percent 
100°F (37.8-C) at 61 percent 98°F (36.7"Q at 70 percent 

For a successful hatch, moisture must evaporate from eggs at just the right 
rate. Small eggs, such as those laid by bantams and jungle fowl, evaporate 
more rapidly than larger eggs. Small eggs therefore hatch better at a higher 

Incubation and Brooding 211 

Good incubator 
sanitation ensures a 

healthy hatch. ^HM^MIM 

Incorrect humidity can cause embryos to die in the shell or chicks to be 
small. Too-high humidity can lead to omphalitis, otherwise known as "mushy 
chick disease." In high humidity the yolk sac does not absorb completely and 
the navel therefore cannot heal properly. Bacteria in the incubator invade 
through die unhealed navels, causing deaths for up to 14 days after the hatch. 

Bringing eggs together from various sources is a sure way to introduce disease- 
causing organisms into your incubator. For healthier chicks, hatch only your 
own eggs. If you must bring in eggs from other sources, fumigate them (see 
page 213). If you sell hatching eggs to a custom hatchery, do not bring chicks 
home from one. 

Good incubator sanitation improves hatching success and gives chicks 
a healthy start in life. It also offers an important way to break the disease 
cycle in a flock. Another way to break the disease cycle is to avoid hatching 

Hatching itself is a major source of incubator contamination. By the time 
the hatch is over, the incubator is littered with organic debris that provides an 
ideal environment for disease-causing organisms. If you practice continuous 
hatching (continuously adding new settings of eggs as previous settings 
hatch), keep a separate small incubator to use for hatching. Thoroughly clean 
the hatcher after each hatch. 

Begin by vacuuming out loose down. Then wipe out hatching debris with a 
damp sponge, or the debris will protect disease-causing organisms from the 
disinfectant. Scrub the hatcher with detergent and hot water, followed by a 
good disinfectant such as Germex or chlorine bleach ( l A cup bleach per gallon 
of hot water, or 30 ml/I). If possible, let the incubator dry in the sun. 

Incubator Sanitation 

212 Thf. Chicken Healti i Handbook 

Clean your hatcher at the end of each 
hatching season. Cleaning and disinfect- 
ing does not destroy all disease-causing 
organisms, but it does make the environ- 
ment less favorable for the survival of any 
microorganisms that remain. If you let 
cleanup go until the beginning of the next 
season, you'll have more microbes to con- 
tend with, harbored all that lime in fluff 
and droppings. 


Commercial and custom hatcheries 
routinely fumigate their incubators to 
minimize the spread of salmonella and 
other bacteria. Small home incubators 
er a serious disease outbreak. Fumigation 
rids an incubator of disease-causing organisms by means of gas that pen- 
etrates cracks and other areas you can't reach with a brush or spray. Prior to 
fumigation, thoroughly clean ha telling debris from the incubator. 

For the fumigant, you will need formaldehyde (CH,0), the most effective 
disinfectant against viruses, but one that works only in an enclosed space. It is 
a toxic, volatile chemical that has a strong odor, is caustic, and irritates the 
eyes. A common brand name is Formalin, formaldehyde mixed with water in a 
40 percent solution (37 percent by weight). You will also need potassium per- 
manganate (KMnO,), a poison that comes in the form of a dry powder. 

These two chemicals are available from drugstores and veterinarians, but 
theft safe use requires knowledge and care. Wear plastic gloves while handling 
them. If you get any on yourself, flush your skin with plenty of water. If you 
normally keep your incubator in the house, move it to an outbuilding for fumi- 
gation. Due to the danger of inhaling the gas, this is not a safe procedure to 
carry out in your living room. 

For mixing the chemicals, you'll need a tall earthenware or enamel con- 
tainer. Do not use metal — the chemicals may eat right through it. Do not use 
glass unless it's Pyrex — the chemical reaction will generate heat that might 
crack regular glass. Use a container ten times larger than the combined vol- 
ume of the chemicals, so none can splash out during the chemical reaction 
that will cause the mixture to bubble up. 

Close all vents to make the incubator airtight. Holding your breadi to avoid 
inhaling poisonous gas, combine the chemicals in die earthenware or enamel 
container and place the container in die incubator, off the floor somewhere 

Styrofoam Incubators 

Although no one has formally 
studied thedifficulty of clean- 
ing styrofoam incubators, 
people using them have expe- 
rienced hatching difficulties 
in successive years in spite of 
sanitation practices that 
would be adequate for a 
wooden incubator. Since dis- 
infectants may not adequately 
penetrate the porous styro- 
foam, fumigation may be the 

Incubation and Brooding 213 

near the center. ( 
cubator door. 

Run the incubator at normal 
temperature and humidity for at 
least 30 minutes, preferably over- 
night. At the end of the fumigation 
period, open the incubator and all 
the vents to let the gas escape. Also 
ventilate the room or outbuilding in 

Determining Chemical 
Amounts lor Fumigation 

To figure out how much of each 
chemical you need, determine the 
cubic footage of your incubator by 
multiplying its length times its 
width times its height. As a general 
rule, use twice as much Formalin by 
liquid measure (ml or cc) as potas- 
sium perm anganateindrymeasure 
(g). For each cubic foot, measure 
out 1 .2 cc Formalin and 0.6 g potas- 
Fumigation of hatching eggs is s j um permanganate (per cubic 
an effective method of controlling meter, 40 cc Formalin and 20 g 
diseases when eggs are brought to- potassium permanganate). Donol 
gether from varying sources (a m ix them together until you're 
common way to spread disease from 
flock to flock) or where valuable 
hatching eggs become dirt)'. 

Fumigating eggs before hatching destroys organisms on the outside of the 
shell. The procedure is the same as for fumigating an empty incubator. If you 
are making only one setting at a time, you can place the eggs in the incubator 
and fumigate both at the same time. If you make weekly settings, fumigate eggs 
before placing them in the incubator, which means keeping a separate incuba- 
tor just for fumigation. If you use a separate hatcher, time your settings so you 
can fumigate new eggs right after the previous hatch. 

If you fumigate eggs during incubation, do so either within 12 hours after 
setting them or after the fourth day. Otherwise, die fumigant may harm em- 
bryos during the early days of development. Commercial and custom 
hatcheries often fumigate again after moving eggs to the hatching incubator 
(but never after eggs have pipped, or chicks may be injured) . Fumigate eggs for 
20 minutes using 0.8 cc Formalin and 0.4 g potassium permanganate per cubic 
foot (26 cc Formalin and 13 g potassium permanganate per cubic meter). 


During incubation, remove eggs that are not developing properly to eliminate 
a potential source of incubator contamination. The first eggs that can be iden- 
tified as developing improperly are infertiles, wbich look clear during candling. 

The cause of infertility may be easy or difficult to identify. Sometimes the 
germinal disc or "zygote" dies between the time an egg leaves a hen's ovary 

214 Tm Chicken Health Handbook 

and (he lime incubation begins — a phenomenon known as "weak fertility." 
Since weak fertility is indistinguishable from infertility, the cause is impossible 
to trace. 

One cause of infertility may be an incorrect ratio of cocks to hens. The op- 
timum mating ratio for lightweight laying breeds is one cock for up to one 
dozen hens; the optimum ratio for heavier meat breeds is one cock per eight 
hens. More hens than diat, and the cocks may not get around to all of diem; 
more cocks than that, and the cocks will be so busy fighting among themselves 
that they won't have time to get around to all die hens. 

Even if the mating ratio is right, fertility will be low in a breeding flock that's 
too closely confined. In a small flock with only one cock, the cock may prefer 
some hens and ignore the others. Hens that are high in the peck order tend to 
be mated less often dian hens lower in peck order. The answer is to either dis- 
rupt the order by rotating cocks or identify and artificially inseminating die 
infertile hens. 

A cock that's too old or too fat may have fertility problems. Frozen combs 
and watties can also cause infertility (see "Frostbite," page 132). A cock with a 
leg or foot injury may have trouble breeding. Never catch a rooster by one leg, 
or you may permanently damage a joint. Excessively showing breeders, cocks 
or hens, can cause stress that leads to infertility. During hatching season, keep 
valuable show birds in the breeding pen. 

Nutrition can affect fertility. Vitamin E deficiency causes a cock's testes to 
degenerate, resulting in reduced fertility or even sterility. Vitamin A deficiency 
also causes reduced fertility in cocks. Cocks with large combs that interfere at 
tlie feed trough may have low fertility. Eggs laid by hens that are underweight 
or overweight may be infertile. Supplementing lay ration with grains during 
the breeding season interferes with vitamin, mineral, and protein balance. 

Diseases that affect fertility include chronic respiratory disease, infectious 
coryza, infectious bronchitis, and Newcasde. Eggs from breeders that have re- 
covered from any of these diseases may be infertile. Marek's disease can cause 
permanent ovary damage that leads to infertility. Parasite problems, internal 
or external, can interfere with fertility. 

Infertility problems may be breed-related. A classic example is low fertility 
caused by the abnormal semen of white Wyandotte cocks with rose or pea 
combs. Heavily feathered breeds such as Brahma, Cochin, Orpington, and 
Wyandotte may have fertility problems unless the feathers are clipped from 
around their vents. Cocks with crests, such as Houdan or Polish, may not see 
well enough to catch wily hens unless their crests are clipped back. 

Season can affect fertility, which tends to be low during times of year when 
daylight hours are fewer than 14. Just as lighting keeps hens laying during short 
winter days, it also improves die fertility of cocks. Fertility is highest in spring 
and drops during the heat of summer. 

Incubation and Brooding 215 


Just because a fertile egg contains a sperm cell, making it potentially capable of 
development during incubation, doesn't mean the egg will survive die 21 days 
of incubation and hatch into a healthy chick. Many things can happen to affect 
the egg's hatchability. 

On average, even a hen hatches only 89 percent of her fertile eggs. Not 
many years ago, 60 percent was considered a reasonable rate for artificial incu- 
bation. Today's improved incubators average 85 percent. By conventional 
definition, anything more than 75 percent of fertiles hatched is considered a 
high rate; less than 50 percent is low. 

If you are hatching in the mid to high range, you can probably improve 
your rate by fine-tuning the way you run your incubator. If your hatches fall in 
the low range, look for other causes. 

The age of your hens may be a factor. The small eggs with small yolks laid 
by pullets are low in hatchability and produce a high percentage of deformed 
embryos. Hatchability rises as eggs reach full size, but drops again by 3 to 4 
percent between a hen's first and second year. Whether hatchability continues 
to drop thereafter is a matter of contention, but hatchability is certainly likely 
to go down in hens that are out of condition, parasitized, or diseased. Hatch- 
ability is especially affected by salmonellosis, which is transmitted through die 
egg and causes embryo or early chick death. 

Salmonellosis and other diseases are transmitted from infected breeders 
to their offspring through hatching egg 

• The infectious organism may enter the < 
an infected hen. 

• Bacteria may get on die shell as the egg is laid or when it lands in a 
contaminated nest. Bacteria then enter the egg through the shell, 
which occurs more readily if the shell cracks or gets wet (for example, 
during improper washing). 

Diseases Transmitted Through Hatching Eggs 

Colibacillosis Infectious stunting Runting syndrome 

Chronic respiratory 

Egg drop syndrome 
Epidemic tremor 
Infectious anemia 

Infectious synovitis 

Lymphoid leukosis 

Rotaviral enteritis 

Viral arthritis 

2 1 6 Thk G-riCKEfy Health Handbook 


tor (often inhaled in fluff) or in the brooder (usually through ingested 
droppings in feed or water). 

Nutritional deficiency is one of the most common causes of poor hatch- 
ability. Lay ration contains less protein, vitamins, and minerals than a breeder 
flock needs, affecting egg composition and resulting in poor hatchability. The 
older the breeders are, the worse the problem becomes. 

In some areas, feed stores car ry breeder ration. In other areas, the closest 
thing is gamebird ration. If you can find neither, feed your flock a handful of 
dry catfood two or three times a week and either add a vitamin/mineral 
supplement to the drinking water or give each bird % cc vitamin AD&E inject- 
able every 3 weeks. Start this regime 6 weeks before you plan to start collecting 
hatching eggs. 

An embryo's appearance, combined with the day on which it died, pro- 
vides a clue regarding which nutrient might be lacking. For example, in 
riboflavin deficiency, deaths peak at three points: the fourth, tenth, and four- 
teenth day of incubation. Embryos may be dwarfed, have beaks that look like a 
parrot's, have unusually short wings and legs, and have clubbed down — a 
condition, seen most often in black breeds, in which the down is clumpy, and 
curls in a characteristic way because die down sheaths fail to rupture. 

Incubation and Brooding 217 

Nutrition-Related Hatching Problems 



Day of Death: 

Early incubation 
4th day 

10th day 
10th -2 1st day 
14 th day 
17th day 
18th- 19th day 
1 9th -21st day 
20th & 21st day 
Late incubation 

At pipping 

vitamin A 
vitamin E 
vitamin B12 
vitamin D 
folic acid 
pantothenic acid 
vitamin E 
vitamin K 
selenium excess 
folic acid 

l excess 

Embryonic Appearance: 

Beak/head zinc 


Beak, short vitamin B12 

upper/lower beak vitamin D 

crooked (parrot riboflavin 

beak) manganese 



Embryonic Appearance (con I.): 

Bones/beak soft 

& rubbery 
Clubbed down 
Eyes pale 


Feathers, abnormal 
black in ermine 
Fluid in body 
Growth, dwarfed 


Legs, bowed 



Navel not closed 
Skull deformed 

Spine poorly 

Incubation time 

too long 

vitamin D 

vitamins A &D 

pantothenic acid 
vitamin D 

vitamin B12 
vitamin D 

vitamins A & D 
vitamin B12 

vitamin B12 







Inbreeding is a sure way to reduce hatchability. Continuous, close in- 
breeding causes a phenomenon known as "inbreeding depression," for which 
low hatchability is usually the first sign. Later signs are fewer and fewer eggs 
laid, and chicks lacking in "constitutional vigor," meaning diey're droopy and 
unthrifty, and may or may not die soon after hatching. 

Inbreeding is unavoidable if you raise an exhibition strain or you're trying 
to preserve one of the fast-disappearing classic breeds. For every 10 percent 
increase in inbreeding, however, you can expect a 2.6 percent reduction in 

218 The Chicken Hlai.i i i Handuook 


Incubation Trouble-Shooting 


cock loo old 
cock too l;u 

cocks have loot/leg injuries 
frozen combs and waitles 
excessive showing of breeders 
eggs stored loo long 
wrong storage temperature 
hens too fat or too thin 
llock too closely confined 

breeder flock unhealthy 
breeder ration low in vitamins 

eggs chilled or heated 
improper fumigation 

irregular incubator temperature 
green appearance aspergillosis 


die day 1-2 

die day 1-7 

die at 12-18 days 

dieal 19-21 days 
(yellowish brown 
Quid in eggs) 

die at 21 days 
(without pipping) 

die at 21 days 

S stored loo long 
irregular incubator temperature 
improper turning 
deficient breeder rations 

temperature too high or low 
poor ventilation 
incorrcci breeder ration 


eggs noi turned properly 
hereditary weakness 
wrong lemperature 

humidity loo low 
lemperature too low 
temporary temperature surge 


use younger cock 
condition cock 
treat injuries 
treat for frostbite 
keep breeders home 
store 6 days or less 
store eggs at 55"PU3"Q 
condition hens 
give breeders more room 

check for parasites and disease: 
feed alfalfa meal and cod liver 

collect hatching eggs often 
do not fumigate between 12th 

and 96th hour 
control lemperature 

do not hatch eggs with 
cracked or poor shells; clean 
and disinfect incubator 
between hatches 

store 6 days or less 
control temperature 
turn eggs at 8-hour intervals 
vitamin-mineral supplement 
obtain new cock 
avoid feeding breeders moldy 

control temperature 
open vents or remove plug 
feed milk, yellow corn, alfalfa 
meal, cod liver oil 

hatch only clean, sanitized 

turn at least 3 times/day 
use stock with high hatchability 
control hatching lemperature 
improve incubator sanitation 

increase humidity 

conirol lemperature 





Embryos (cont.): 

die ai 21 clays 
(pipped and 

die at 2 1 days 
(pipped, bu( chicks 
too big to work out 
of shell) 





can't get Tree of 

sticky, shells 

sticky, smeared 
with yolk 

rough navels 


short down 

splayed legs 
crooked toes 
big, soft, weak 

unabsorbed yolk 

mushy and smell 

crossed beaks 


poor hatching ventilation 

high incubation temperature 

low incubation temperature 

temperature too low 
power outage 

eggs stored too long 

hatching humidity too low 
hatching temperature too high 

ton much hatching ventilation 
hatching humidity too low 

hatching temperature too low 
hatching humidity too high 

hatching temperature too high 
temperature fluctuation 
hatching humidity too low 

eggs too small 
humidity too low 
temperature too high 

temperature too high 
humidity too low 

temperature too high 

temperature too low 

temperature too low 
poor ventilation 

hatching humidity too high 



hatch only clean, sanitized eggs 
hatch eggs only from typhoid- 
clean breeders 

open vents or remove plug 

decrease temperature W 

increase temperature V4" 

increase temperature 

cover incubator during power 

store 6 days or less 

increase hatching humidity 
decrease temperature 16" at 

hatching time 
reduce vent openings 

increase hatching humidity- 
increase hatching temperature 
open vents or remove plug 

decrease hatching temperature 
check wafer in incubator 
increase hatching humidity 

hatch only normal-sized eggs 
increase humidity 
decrease temperature 

decrease temperature 
increase humidity 

decrease temperature 

increase temperature 

increase temperature 
open vents or remove plug 

decrease humidity 
sanitize incubator 
cull breeders 

220 The Chicken Health Hanouook 

due to failure to reproduce. A flock can become extinct after only six to eight 
generations of brother-sister maiings. 

Inbreeding depression has two distinct causes: concentration of genetic 
factors and the inbreeding itself. You can therefore slow the decline and im- 
prove reproduction in two ways. First, by selecting and culling for number of 
eggs laid, hatchability of the eggs, and vigor of the resulting offspring. Second, 
by using less close matings that result in more gradual inbreeding — making 
fifty birds the minimum size lor an inbred tlock. 

Better yet, occasionally introduce birds from a different strain. Mating 
birds from different strains invariably results in hybrid vigor. The opposite of 

creased viability, and improved productivity. 

Lethal Genes 

One result of inbreeding is concentration of lethal genes — recessive genes 
that show up only when two birds with die same trait are mated. Many lethals 
are related to specific breeds. 

Japanese chickens carry the most widely studied lethal, the creeper gene, a 
trait that was once valued in broody hens because it causes short legs and 

mated to a cock carrying the creeper gene, one-quarter of the chicks die during 
die first week of incubation. 

Dark Cornish carry a similar short-leggene that causes death at the time of 
hatch. Signs of "Cornish lethal" include short beaks and wings, and bulging 

New Hampshires carry a lethal that causes death in the twentieth and 
twenty-first day of hatch. Signs are crooked necks, short upper beaks, and 
shriveled leg muscles. 

The silver gray Dorking has a lethal that causes deadi in the ninth day of 
incubation. Embryos have short necks and beaks. 

A Barnvelder lethal causes "Donald Duck syndrome," in which the upper 
beak curls upward, the lower beak curls downward, and death occurs in the 
last days of incubation. 

Ancona, Plymouth Rock, Rhode Island Red, white Leghorn, and while Wyan- 
dotte. Chicks hatch but can't control their neck muscles. When a chick uies to 
stand, its head falls over and the bird falls down. Unable to eat or drink, it dies 
soon after hatching. 

This is by no means a complete list of all die possible lethal genes. Among 
other lethals are those found in the black Minorca (short legs widi extra toes), 
Rhode Island Red (short legs, wings, £ 

Incubation and Brooding 22 1 

parrot-like beaks), and white Wyandotte (early embryonic deadi). Two com- 
mon genetic factors that don't qualify as lethal genes, but that do reduce 
hatchability, are frizzledness and rumplessness. 

One way to avoid the effects of lethal genes is to avoid mating closely re- 
lated birds. Another way is to deliberately mate related birds and try to ferret 
out and cull breeders earning lethal genes. 

Genetic Defects 

Two common hereditary defects, wry neck and wry tail, are caused by re- 
cessive genes, meaning diey show up only when two birds are mated diat carry 
the same gene. 

Wry or twisted neck, resulting from curvature of the spine or "scoliosis," 
occurs as birds grow, and is particularly common among brown Leghorns. It 
usually happens to a group of related birds and does not affect their ability to 

Wry or twisted tail is a condition in which the tail feathers lean or twist to 
one side due to weakness in the vertebrae that hold die tail. Wry tail usually 
shows up as the tail feathers grow and become heavy. 

Do not use birds wii h either of these defects as breeders. Cull breeders you 
can identify as carrying these recessive genes. 

Chick Identification 

You can't idem 

offspring. Chicks can be tracked in one of two ways: embryo dyeing and loe- 
punching. Embryo dyeing works best on chicks with white or light-colored 
down, and wears off as soon as the chicks grow their first feathers. Toe- 
punching works for all chicks and is permanent. You might want to combine 
the two techniques, dyeing embryos so you can toe-punch chicks diat get 
mixed up during the hatch. 

Injecting dye into eggs before they hatch lets you color-identify chicks 
from different matings. Dyeing in no way affects a chick's health or growth 
rate, provided you handle the eggs carefully and use only clean materials. 

You will need a 20-gauge, 1-inch (25mm) long hypodermic needle, a sharp 
sewing needle of the same size or a little bit bigger, and a set of food dyes in 2 or 
3 percent concentration (sold at most grocery stores). Among the primary col- 
ors, red, green, and blue show up best. Purple, made by combining red and 
blue, also works well. Yellow and orange don't show up well at all, since chick 

222 The Ciiicki:n Hkalth Handbook 

down is often yellowish to start with. 

Embryos dye best during the eleventh to fourteenth day of incubation. To 
avoid chilling the eggs, remove no more eggs from the incubator than you can 
dye within 30 minutes. 

About V2 inch (13 mm) from the pointed end, disinfect an area about the 

size of a quarter by wiping it with 95 
percent rubbing alcohol or 2 percent 
tincture of iodine. Dip the sharp 
needle into the alcohol or iodine. 
Cushioning die egg in one hand, make 
a tiny hole in the center of the disin- 
fected area by pressing against it with 
the needle, twisting the needle back 
and forth until it just penetrates the 
shell and membranes. Take care to 
make only a tiny hole that does not go 
deeper than necessaiy to pierce the 
inside membrane (no more than l fi> 
inch or 3mm). 

Dip the hypodermic needle into 
the alcohol or iodine and fill it with Vz cc of dye. Insert it into the hole so the tip 
is just beneath the inner shell membrane. Very slowly depress the plunger to 
release the dye without letting it overflow. To avoid mixing two colors, use a 
clean needle if you change dyes. 

Seal the hole with a drop of melted paraffin or a tiny piece of adhesive ban- 
dage (Sheer Strip sticks best). Return the eggs to the incubator. 


A toe-punch, available from many poultry supply catalogs, is about the 
size of fingernail clippers. It functions like a paper-hole punch and is used to 
remove the web between the toes of a newly hatched chick. As die chick grows, 
you can identify its parentage by the pattern of its punched-out webs. 

When chicks are dry and ready to come out of the incubator, hold each 
gently but securely in one hand with one foot extended. Carefully position the 
punch over the web. With one firm stroke, punch away the web. Don't just 
punch a hole through the web, or the web may eventually grow back. 

The pattern of removed webs lets you identify chicks from up to sixteen 
different matings. Here's how it works: on each foot, a chick has three main 
toes and therefore two webs — the outer web (between the middle and outside 
toe) and the inner web (between the middle and inside toe). 

Starting at the chick's left side, die first web (left outer) stands for 1; the 

Incubation and Brooding 223 

next web (left inner) stands for 2; the next 
web (right inner) stands for 4; the far right- 
hand web (right outer) stands for 8. Assign 
each mating a number from 1 to 15 and 
identify chicks from each mating by add- 
ing up the numbers corresponding to the 
punched webs. (For a sixteenth mating, 
leave the chicks unpunched.) 

Chicks in batch number 1 have die left 
outer web punched. Chicks in batch num- 
ber 2 have the left inner web punched. 
Chicks in batch number 3 have both the 
left outer and left inner webs punched (1 + 
2 = 3). Chicks in batch number 5 have the 
left outer and right inner webs punched ( 1 
+ 4 = 5). And so forth. 

Toe-punching works only if you know 
when you open the incubator which 
chicks came from which mating. You can 
identify chicks by: 

• dyeing embryos 

• hatching different matings at 
different times 

• keeping eggs from different 
matings on different hatching trays 

Toe punch patterns 

upside-down baskets (pedigree 
baskets) such as plastic pint-size fruit 

Left Foot 

/light Foot 

\o\ / 


\ I / 

\ \ol 


\ ! / 



\ ! / 

\ 1 / 


\o| / 

\o| / 


\o| / 

\ \o/ 


\o| / 



m / 

\ ! / 


\ o/ 

Vol / 


\ o/ 

\ |o/ 


\ o/ 



\ jo/ 

i i / 



\oj / 



\ |o/ 






\ 1 / 


\ 1 / 


The typical death rate among chicks is 5 percent or less during the first 7 weeks, 
up to half of which usually occurs during the first 2 weeks. As distressing as 
occasional deaths among chicks can be, they're nothing to be concerned 

On the other hand, stress caused by chilling, overheating, dehydradon, or 
starvation, or any combination tiiereof, can drastically reduce the immunity of 
newly hatched chicks, making diem susceptible to diseases they might other- 
wise resist. As soon as you remove cliicks from the incubator, place them in a 
clean carton or disinfected brooder. 

224 The Chicken Health Handbook 

Chilling or overheating can occur if the brooder is too cool or too warm. 
You can telJ chicks are comfortable when they are evenly distributed in the 
brooder. If they crowd to the corners, they are too warm. If they crowd beneath 
die heal source, they are cold. Brooding chicks at too cool a temperature in- 
creases their susceptibility lo salmonella infections. Start the brooding 
temperature at approximately 95°F (35"Q and reduce it 5°F (3°C) each week 
until you reach room temperature. 

Smothering cm occur if chicks don't get enough heat or are placed in a 
draft, causing them to pile on lop of each other to stay warm. As a result, the 
chicks on the bottom may be smothered. Smothering due to drafts or insuffi- 
cient heat usually occurs at night. It can be prevented by placing a cardboard 
ring around the chicks during their first week of life, which keeps them near the 
source of heat and out of corners. Smothering also occurs when chicks are 
transported in stacked boxes with too few ventilation holes, or in the trunk of a 
carwhereaircirculation is poor. In older chicks, piling may be caused by fright, 
especially if they've been moved to unfamiliar housing. When you move chicks 
to new housing, keep on dim lights and check the chicks often during the first 
few nights. 

Crowding causes litter to become hard-packed and caked with droppings. 
Pads of litter and droppings may stick to the chicks' feet, causing crippling 
and/or infection. In crowded conditions, litter may have a strong odor, usually 
of ammonia. Severe ammonia fumes cause chicks to sit around with their eyes 
closed. If crowding is not corrected, chicks' eyes may become inflamed. 

Feather- and toe-pickingmay result from crowding or from a diet too low 
in protein. Commercial chick starter usually contains enough protein to pre- 
vent picking. For more details, see "Cannibalism," page 135. 

Brooder Diseases 

Disease is usually not a problem in newly hatched chicks unless either 
they contract an egg-transmitted disease during incubation or the brooder en- 
vironment is contaminated. The brooder may become contaminated either 
because it was not thoroughly cleaned after die last batch of chicks or because 
disease-causing organisms are being shed by chicks with an egg-transmitted 
disease, passing the disease on to other chicks in the brooder. 

Since adult birds are reservoirs of infection (whether or not the adidt birds 
themselves are sick), brood chicks away from older birds to give them time to 
develop natural immunities. Natural immunity is die result of gradual expo- 
sure to infectious organisms, rather than exposure to a high concentration that 
can cause disease instead of immunity. 

The age at which chicks first show symptoms gives you a clue as to what 

Incubation and Brooding 225 

age group. If your chicks get sick, look for a disease in their age group that most 
closely matches their symptoms. If you can't find a good match, consider dis- 
eases that are common in chicks slightly younger or older than yours. 

The most common brooder disease, especially in warm humid weather, is 
coccidiosis. If you brood chicks in a temperate climate, or you hatch late in the 
season, prevent coccidiosis by using medicated starter ration containing a 
coccidiostat from day 1 to 16 weeks. 

Brooder Nutrition 

Slow growdi in chicks can result from nutritional deficiencies that are all 
too common in breeder- flock diets. General signs of deficiency are poor 
growth and lack of vigor. All chicks up to 3 weeks old, especially chicks that 
have been shipped, benefit from the addition of a vitamin supplement in their 
drinking water. 


Starvation or "starve-out" results when chicks don't start eating widiin 2 to 
3 days of hatch, causing them to get too weak to actively seek food. Starve-out 
can occur when shipped chicks are in transit for too long, so that they become 
weak before they are offered feed. It can also be caused by feeders that are 
placed where chicks can't find them or by feeders that are so high chicks can't 
reach them. 

Other causes are excessive heat over feeders diat drives chicks away, and 
using sand or sawdust as litter for newly hatched chicks. To keep chicks from 
eating litter instead of feed, cover the litter with paper toweling or burlap until 
chicks start eating well. 

226 The Chicken Health Handbook 

chicks are 
and perky. 


Chicks will die if they do not start drinking by the time they are 4 days old. 
Chicks that can't find water don't grow at the proper rate, develop bluish 
beaks, and stop peeping. Deaths start occurring on the fourth day and con- 
tinue until the sixth day. If water is available, but some chicks can't find it, the 
ones surviving after the sixth day are those that found the water. 

[f chicks have been shipped, make sure they know where to find water by 
dipping each beak into the fount as you transfer birds from the shipping carton 
to the brooder. Do not place the waterer on a platform where chicks can't 
reach it. If you switch from one waterer to another, leave the old waterer in 
place for a few days until the chicks get used to the new one. Stick your finger 
into the water to make sure a bad electrical connection isn't causing chicks to 
get a shock each time they try to drink. 

Slipped Tendon 

Slipped tendon, properly known as "perosis," may result from brooding 
chicks on paper or other slick surfaces. It occurs most often in heavy and fast- 
growing breeds, and may be caused either by hereditary factors or improper 
nutrition. If the cause is manganese deficiency, the problem should clear up 
after 1 month of feeding the chicks a supplement containing manganese. 
(Slipped tendon is described more fully in chapter 15). 

Crooked Toes 

A chick with crooked toes walks on the sides of its feet, causing the toes to 
accumulate manure clumps and/or develop sores. Chicks can have crooked 
toes if humidity was low during incubation or the brooder floor is cold. For 
unknown reasons, crooked toes have been associated with infrared brooding 

Incubation and Brooding 227 

and wire floors. They may also be hereditary, occurring most often in heavy 
breeds, especially in males. If you can't identify a cause, don't keep crooked- 
toed chickens as breeders. 

Crooked toes can be < 
from curled-toe paralysis caused by riboflavin 
deficiency. In die former condition, toes twist 
to the side but the chick can still walk fine. In 
curled-toe paralysis, the toes curl under, caus- 
ing the chick to walk on the tops of its toes. 
Because walking is difficult, die chick spends a 
lot of time resting on its hocks. 

Curled-toe paralysis can occur where 
breeder hens are fed unsupplemented lay ra- 
tion. The chicks grow slowly and may have 
diarrhea during their first week or two of life. 
In a severe case, the toes curl completely back and the legs become so weak the 
chicks walk on their hocks. Deaths occur after about 3 weeks. 

If the starter ration (rather than breeder ration) lacks sufficient riboflavin, 
symptoms will occur when chicks are 10 to 14 days old. An early warning sign is 
alert chicks that can't stand up. If you supply a multivitamin supplement in the 
chicks' water before their feet are permanently damaged, they should recover 
in 2 to 3 days. 

Crooked toes can also be caused by flexing of the toes due to vitamin E 
deficiency, a condition known as "encephalomalacia" (sometimes called 
"crazy chick disease"), described fully in chapter 15. 

Chick wilh curled toe paralysis 

Brooding Deficiencies 

When vitamin A is deficient in the chicks' ration, the birds won't grow and 
will appear drowsy, weak, uncoordinated, and emaciated. They will have 
ruffled feathers, will stumble and stagger when they tiy to walk, and may have 
dry, dull eyes. 

Thiamin (vitamin B 1 ) deficiency in starter ration shows up suddenly when 
chicks are 2 weeks old and lose their appetites. As they lose weight, their feath- 
ers ruffle, they develop weak legs, and they become unsteady on their feet. 
Progressive paralysis starts at the feet and works upward, until chicks sit back 
on their hocks with their heads pointed upward (the so-called "star gazing" 
posture). Chicks given an oral thiamin supplement may recover. 

In riboflavin (vitamin B2) deficiency, chicks continue to have good appe- 
tites but grow slowly and become weak and emaciated. They may have 
diarrhea, droopy wings, and dry skin. They are reluctant to move, doing so by 
walking on their hocks with the help of their wings. 

Pyridoxin* (vitamin B6) deficiency causes chicks to walk with jerky move- 

228 The Chicken Health Handbook 


Nutritional Problems in Chicks 



Beak, crusty 



clots slowly 

Bones, soil 

Breast, muscles, 
(white muscle 

Droppings, soft 

Eyes, dry/dull 
scabby or crusty 

stuck together 


(star gazing) 

Feathers, black 
in brown or red 
lack color 

long or uneven 

rough and 


Feet, bottoms 
rough and 
toes curl 


pantoihenic acid 

vitamin K 
vitamin UI2 
vitamin K 

vitamin D 

selenium & 
vitamin E 


vitamin A 

pantothenic acid 
vitamin A 

vitamin D 

folic acid 

amino acid 
folic acid 

pantoihenic acid 

vitamin A 


pantothenic acid 


Deficienc} 1 / 

Legs, short /thick 


hocks enlarged 

(white muscle 

Mouth, inflamed 
(black tonglie) 


excessive fl ight 
jerky movements 




Skin, dry 

greenish fluid 

Wings, droopy 





folic acid 


nicotinic acid 





selenium & vitamin E 



vitamin E 

vitamin A 
vitamin E 

vitamin A 

folic acid 

selenium & vitamin E 


InCUUATKKN \NI) B[i()()l)IN(, 229 

ments. They may run around flapping their wings, then fall onto their sides or 
backs, jerking their heads and legs. Pyridoxine deficiency is similar to 
encephalomalacia, except diat here the nervous activity is much more intense 
and ends in exhaustion and death. 

Folic acid deficiency causes poor growth, anemia (skin appears pale), and 
slipped tendon. It can cause lack of feather color in Rhode Island Red and 
black Leghorn chicks and poor feathering in any breed. 

Vitamin E deficiency causes chicks to stumble and stagger when they 
walk. A serious deficiency may result in encephalomalacia, exudative 
diathesis, or white muscle disease (all described in chapter 15). 

Vitamin /(.'deficiency causes a chick's blood to clot slowly, so the chick may 
bleed to death from a relatively minor wound. Chicks will be deficient in vita- 
min K if the breeder-flock diet was deficient. 

Chickens and Human Health 

THE CHANCE THAT YOU WILL GET A DISEASE from your chickens is pretty 
slim, especially if you practice common sense hygiene that includes washing 
your hands after working in or around your hen house. Many of the organisms 
that cause the diseases described in this chapter are fairly common in the hu- 
man environment, whether or not that environment includes chickens. 
Ordinarily, those organisms cause no problems. Exceptions are in people with 
impaired immune systems or low resistance due to systemic dierapy (immu- 
nosuppressive or antibacterial therapy, for example), pregnancy, obesity, 
diabetes, or some disease unrelated to chickens. 

The low risk of getting any of diese diseases is no consolation to those few 
who might be infected. This chapter, then, is offered in die spirit of helpfulness 
— physicians lend to overlook or misdiagnose diseases they don't often see. If 
you visit your doctor about a condition you suspect might be related to your 
chickens, mention your concern to your doctor. 

Although many of these diseases have sources other than the poultry envi- 
ronment, the focus here is on their relationship with chickens. Diseases that 
humans can get, directly or indirecdy, from chickens can be broken down into 
four categories: environmental, parasitic, zoonotic, and toxic. 


Chickens and Human Health 231 


Chicken Disease 

Risk of Human Infection 

tlN ViKUWJvlcIN 1AL 





l must] 




very low 

Farmer's Lung 



Hen Worker's Lung 



1 listoplasmosis 


very low 



extremely low 










extremely low 



extremely low 













extremely low 







extremely low 

Necrotic enteritis 






Paratyphoid (E enteritidis) 


Staph poisoning 


extremely low 

Environmental Diseases 

It is possible for humans to contract some infections from the same sources as 
chickens, the result of environmental exposure rather than inter-species con- 
tagion. Most human diseases caused by the poultry environment are mycoses 
or fungal infections. 


Aspergillus fumigahis fungus is quite common in both poultry and human 
environments, but infection is more common in chickens than in humans. 
Humans get infected by inhaling spores from decaying litter. It is a rare disease 

232 The Chicken Health Handbook 

that affects primarily people with low resistance or compromised immune 
systems, in whom the infection can be serious and occasionally fatal. In others, 
the usual result is allergic bronchitis (a respiratory disease characterized by 
coughing), usually successfully treated with anti-asthmatic drugs. 

Aspergillus fltiPUS, found in moldy grains, peanuts, and manioc (fed to 
both chickens and humans), produces a poison dial has been implicated as 
die cause of human liver cancer in tropical Africa and Asia, where die fungus is 


Candida albicans yeast commonly lives in the bowels of humans, chick- 
ens, and many other animals. Infection is transmitted by direct contact with 
yeast in droppings and is usually superficial, except in people with low resis- 
tance or compromised immunity. Infection may involve the mouth (children), 
the genitals (adults), or the skin under fingernails (all ages), resulting in an 
itchy rash that eventually swells with pus. It can be treated with an anti-fungal 
powder or cream (such as nystatin) and corticosteroid cream (such as hydro- 


Cryplococcocus neofonnans is a fungus found worldwide in bird environ- 
ments (more commonly birds odier than chickens). The fungus is not known 
to infect chickens, but on rare occasions does cause infection in humans. It 
inflicts primarily men between the ages of 40 and 60, particularly those who 
use steroids, have Modgkin's disease, or odierwise have suppressed immune 

Infection can be acute or chronic and may affect the brain or lungs, or be- 
come systemic and affect the entire body. The most likely result of inhaling the 
fungus is meningitis or inflammation of the brain covering. Symptoms incl ude 
headache, stiff neck, blurred vision, and confusion, leading to coma and death 
if not treated with anti-fungal drugs. Inhaling the fungus may cause growths in 
the lungs. Symptoms of lung infection are chest pain and coughing, some- 
limes involving phlegm. Lung cases usually clear up on their own. 

Hen Worker s Lung 

Hen worker's lung is an allergic reaction to blood protein and droppings 
inhaled in poultry dust. Few people develop this disorder, which usually re- 
quires prolonged exposure such as a professional poultry worker might 
experience. Symptoms may come on suddenly, approximately 6 hours after 

Chicki \s wi> Human Health 233 

exposure. They include difficult or painful breathing, cough, fever, chills, and 
sometimes loss of appetite, nausea, and vomiting. The symptoms, easily mis- 
taken for flu, may last several hours or up to 2 days, although complete 
recovery may take weeks. 

The allergy sometimes develops gradually, starling with bouts of breath- 
ing difficulties and coughing that increase in frequency and severity. The 
allergy occasionally takes a chronic form, resulting in difficult or painful 
breathing brought on by physical activity, accompanied by the coughing up of 
phlegm, extreme fatigue, and gradual weight loss. If corrective measures are 
not taken, die end result may be respiratory failure. 

This disease is difficult to diagnose. The primary clue is the relationship of 
symptoms to exposure — for example, professional workers who experience 
relief during their days off. Backyard keepers may experience symptoms 4 to 8 
hours after exposure, something that can be hard to determine if you visit your 
coop two or more times a day. Although frequent attacks reduce the lung's 
elasticity and eventually cause scar tissue, an early chest x-ray may appear nor- 
mal, leading to a possible misdiagnosis of heart condition. 

Hen worker's lung can usually be cleared up by avoiding the poultry envi- 
ronment. Complete recovery is possible if avoidance occurs before lung tissue 
becomes scarred. Whether or not you suffer from hen worker's lung, it makes 

during cleanup, and to install a fan to remove floating dust particles from the 

Farmer's Lung 

Farmer's lung is an allergic reaction similar to hen worker's lung, but 
caused by die spores of Micropolyspora faeni or Thennoactinomyces vulgaris 
inhaled from moldy grains or litter. The allergy typically occurs in areas of high 
rainfall, usually toward the end of winter following a wet summer. Symptoms 
are nearly identical to those of hen worker's lung. Prevention involves wearing 
a face mask when working in dusty areas and avoiding die storage of moist 
litter or grain over winter. 


Inhaled Histoplasma capsulation spores from old, dry chicken droppings 
while cleaning or dismantling an old chicken house (or while working in in- 
fected garden soil) can cause a rare though potentially serious infectious 
fungal disease. Histoplasmosis occurs mainly in die Ohio and central Missis- 
sippi river valleys where the altitude is low, rainfall is 35 to 50 inches a year", and 

temperatures remain even. Infection does not spread from birds to humans. It 

234 The GHtfcKEN Health Handbook 

usually occurs only in someone who inhales large numbers of spores or who 
has an immunodeficiency disorder. 

Histoplasmosis settles first in the respiratory system and may produce no 
symptoms (other than an abnormal chest x-ray) or may cause symptoms 
virtually identical to those of flu — fever, coughing, joint pains, and general 
discomfort. In patients with suppressed immunity, the disease may spread 
throughout die body, requiring treatment with anti-fungal drugs to prevent a 
fatal outcome. 

Most cases require no treatment — the disease usually clears up on its 
own. Avoid infection by misting litter to control dust before cleaning your coop 
and by wearing a respirator or a dampened handkerchief over your mouth and 
nose while you work. 


Pseudoinonas aeruginosa bacteria are commonly found in soil, pardcu- 
larly in humid environments. In the rare case where chickens become 
infected, their contaminated meat decays rapidly. Human infection is ex- 
tremely rare and most likely to occur through an open wound or a deep 
puncture, typically to the foot. The puncture turns purplish-black toward the cen- 
ter with a reddened area around die outside, and requires antibiotic treatment. 

Parasitic Diseases 

a chicken. 8 ' 8 

Mites and Ticks 

Mites may crawl onto your body if you handle infested chickens, but they 
usually won't stay long. Minimize discomfort by taking a shower and washing 
your clothing. 

A tick can also get on you from a chicken. If the tick bites, it might possibly 
transmit a disease such as tick paralysis (characterized by loss of appetite, 
weakness, lack of coordination, and gradual paralysis) or Rocky Mountain 
spotted fever (characterized by severe headache, chills, muscle pains, and 

If you find a tick trying to burrow into your skin, grasp it widi a pair of 
tweezers and pull until it releases its hold — pull gently but firmly so you nei- 
ther crush the tick nor break its body away while its head remains in your skin. 
Disinfect the bite widi rubbing alcohol. See your doctor if you experience any 
symptoms of a tick-borne disease. 

CmcktNs and Human Hi ai hi 235 


You aren't likely to get infested by worms from your chickens, since 
most worms that prefer poultry do not invade humans. You can, however, 
accidentally ingest worm eggs if you eat without washingyour hands after 
handling contaminated soil or litter. Such an infestation causes few or no 
symptoms and is easy to treat with an appropriate anthelmintic. 

Toxoplasma gondii protozoa rarely infect chickens and even more rarely 
infect humans. Toxoplasmosis results from eating raw or undercooked meat 
of infected chickens (or other animals). Infection usually causes no ill effect, 
except in people with immunodeficiency disorders and in unborn children. 
One- third of the pregnant women who get toxoplasmosis during pregnancy 
pass it to their unborn children, resulting in serious damage [such as blindness 
or retardation), miscarriage, or stillbirth. 

The most common symptoms of toxoplasmosis are fatigue, low fever, and 
muscle pains. The disease is self-limiting and usually goes away on its own. 
Extremely rare are serious cases involving vital organs (eye, brain, or heart), 
which may be diagnosed through blood tests and treated with antimalarial 
and sulfa drugs. 


Many diseases are species specific, meaning they affect only one species, 
whether it be chickens, humans, or some other animal. A few diseases, called 
"zoonoses," are shared by animals and humans. Some chicken diseases are 
caused by zoonotic organisms — creatures so flexible diat they can adapt to 
the human species. Don't be too quick to suspect you have a zoonosis unless 
your chickens have been positively diagnosed as having the disease. 


Humans can contract chlamydiosis, a rare form of pneumonia, by inhal- 
ing dust from feathers or dried droppings of infected birds. The disease was 
first recognized in psittacine birds (parrots), and so was called "psittacosis" or 

is sometimes called "ornithosis." 

Virulent strains appear in cyclic fashion, but not every avian outbreak 
causes human illness. The two most likely causes of chlamydiosis in humans 

s, mor 

236 The Chicken Health Handbook 

lution: wet feathers before plucking), and exposure to 

(improve ventilation and wear a dust mask and gloves). 

The incubation period (time between exposure and first symptoms) is 1 to 

2 weeks. Symptoms include loss of appetite, fever, chills, severe headache, dry 
cough, constipation, muscle stiffness, and sensitivity to light; sometimes rash, 
diarrhea, and vomiting. Early symptoms may be easily confused widi flu or 
other forms of pneumonia. Left untreated, chlamydiosis can be fatal, espe- 
cially in those over the age of 50, but usuall y clears up after 1 days of antibiotic 


Humans who handle vaccine for Newcastle disease often suffer from 
conjunctiviUs (eye inflammation) within 1 to 4 days. Conjunctivitis can also 
occur in those who butcher infected birds and, much less likely, those who 
treat sick chickens. The virulence of Newcastle disease in chickens has no 
bearing on whether or not humans become infected. Symptoms are itchy, red, 
watery, sometimes swollen eye (usually only one). No treatment is known. Re- 
covery is spontaneous and complete, usually in 4 days, but may take as long as 

3 weeks. 


wound on a person who handles or slaughters infected birds. Infeciion u 
appears within a week as an itchy, burning, raised and hardened purplish-red 
patch on the hand that may gradually grow larger. 

Infection is most likely to occur in butchers, kitchen workers, veterinar- 
ians, and artificial inseminators — more often those handling fish, pork, and 
turkey than chickens. The infection is self-limiting. Treated with penicillin, it 
usually clears up within 2 to 3 weeks. 


Listeriosis is more common in animals other than chickens, and is even 
rarer in humans. It is, however, life threatening to senior citizens over the age 
of 70 and to unborn children infected through their moflner's blood. The dis- 
ease spreads to humans who handle or butcher infected birds or who eat 
improperly cooked infected meat. 

Symptoms range from mild skin irritation, to fever and muse 
meningitis I" 

Chickens and Human Health 237 

infected birds, is conjunctivitis (eye inflammation). 

Diagnosis requires blood tests — be sure to tell your doctor you suspect 
listeriosis, or the lab won't think of looking for Listeria. The disease is easily 
treated widi antibiotics. 

Meat and Egg Contamination 

One of the reasons people raise their own chickens, even though doing so costs 
more than purchasing store-bought meal and eggs, is due to concerns about 
pesticide and herbicide residues, bacterial contaminants, and antibiotics in 
commercial poultry products. Sadly, no one is seriously guarding the safety of 
our meat and egg supply. Even the physician who oversees the food-borne- 
diseases branch of die Centers for Disease Control and Prevention, Dr. James 
Hughes, has been quoted as saying, "We've got die most rudimentary surveil- 
lance of food-borne diseases you can imagine." The CDC tracks and reports 
on food-borne illnesses, but docs little to control them. 

Pesticides and herbicides are used on most feed crops that make up 
chicken rations. Unless you have a source of so-called organic rations, your 
eggs and chicken meat will contain no less residue from pesticides and herbi- 
cides than commercial meat, which in any case is extremely low. 

Antibiotics at low levels, along with growth- promoting hormones, are 
used commercially to make chickens reach market weights faster and with 
lower feed costs. You can easily avoid antibiotics and hormones in home- 
grown meat by not making diem part of your management routine and by 
observing the withdrawal period for any drug you use for therapeutic pur- 

Bacteria pose the greatest threat among contaminants in poultry meat or 
eggs, especially those that are commercially produced, since large-scale pro- 
duction lends itself to unsanitary practices. Homegrown meat birds, by 
contrast, are usually killed and cleaned individually, are rinsed under a run- 
ning faucet (rather than in a vat of rapidly contaminated water), and are 
refrigerated promptly; similarly, homegrown eggs are exposed to fewer 
sources of contamination. Nonetheless, remaining aware of the dangers of 
bacterial contamination is the first step toward avoiding them. 

Food-Borne Bacteria 

If meat or eggs are held at room temperature for too long, any bacteria 
present will proliferate. Some multiply more rapidly than others. Since there's 
no way to tell whether or not bacteria are present, you can't go wrong if you 
always handle meat and eggs as if they are contaminated. 

In a healthy adult, bacterial food poisoning is usualJy little more tiian an 

238 Ti -in Chicken Healti i Handbook 

Food-Borne Bacteria 

Infective Toxic 

Campylobacter jejuni 


Clostridium botuliiiuni 


C. perfiingeus 


Escherichia coli x 


Salmonella enteritidis x 

Staphyloccus aureus 


annoyance. In the very young, the 
aged, or someone with a weakened 
immune system, however, bacterial 
food poisoning can be serious or even 
fatal. General symptoms are loss of 
appetite, nausea, vomiting, abdomi- 
nal cramps, and diarrhea that comes 
on suddenly. In many cases, illness 
strikes a group of people who have 
shared a tainted meal. 

Most cases are resolved with bed 
rest and plenty of fluids. For most people, the most serious consequence is loss 
of body fluids and salts (electrolytes). Since symptoms resemble die flu, most 

plicated by odier factors, antibiotics may be of little help and may actually 
make matters worse. 

The most common causes of bacterial food poisoning are Campylobacter, 
E. coli, and Salmonella. Some food-borne bacteria are infective — diey cause 
disease by invading the intestine wall. Others produce toxins that inhibit nutri- 
ent absorption. Some work both ways. 

Egg Sanitation 

A freshly laid egg is warm and moist, and therefore attracts bacteria and 
molds that exist in die poultry environment. After leaving a hen's warm body, 
the egg immediately starts to cool. As its contents contract, a vacuum is created 
that can draw bacteria and molds through the 6,000-plus pores in the shell, 
potentially causing egg spoilage and human illness. 

Eggs produced at home in a clean environment, collected often and 
promptly placed under refrigeration (after cracked or seriously soiled eggs are 
discarded), rarely pose a health problem. Eggs that are slighdy soiled widi dirt 
or dried droppings should be dry cleaned with fine sandpaper. Improperly 
washing them can do more harm than good. 

Eggs produced in a not-so-clean environment and (hose destined for mar- 
ket may need to be washed. Market eggs are often subjected to storage 
temperatures that are higher than desirable (causing bacteria and mold on the 
shell to multiply) and to repeated warming and cooling (drawing more micro- 
organisms through die shell each time). 

If you wash eggs, use water that is 20'F (11"C) warmer than the eggs are, 
otherwise vacuum action may draw microorganisms through the shell or tiny 
cracks may develop in the shell that expose eggs to invasion by bacteria and 
molds. Wash eggs with detergent (not soap) to remove soil. Rinse them in wa- 


number of microorganisms on the shell (the sanitizer won't eliminate all bac- 
teria and mold). If you wash a large number of eggs, change the wash and rinse 
solution often, since both rapidJy become contaminated. 

Sanitizers that will not introduce off odors, colors, or flavors include chlo- 
rine solution (such as Clorox bleach) and quaternary ammonium compounds 
or "quats," used at the rate of 100 to 200 parts per million. Don't get carried 
away and combine chlorine and a quat, or they'll counteract each other. 

Dry eggs thoroughly before placing them in cartons, since wet shells more 
readily pick up bacteria. 


Salmonella bacteria can be found almost everywhere. You would have a 
hard time finding meat, eggs, or any other food that did not harbor one of tfie 

cur each year. No one knows the exact number, since not all cases are reported. 
Only about 5 percent of all cases can be traced to chickens. 

Over 150 different salmonella strains that produce paratyphoid infections 
in chickens cause serious illness in humans. In the 1960s, outbreaks of salmo- 
nella poisoning from bacteria in eggs resulted in institution of the Egg Products 
Inspection Act in the United States. Among other things, the Act removed sub- 
standard non-Grade A (cracked or "check") eggs from die marketplace. For a 
time, fewer incidence of salmonellosis in humans were reported. 

Since the 1960s, however, an especially virulent, antibiotic-resistant strain 
of S. enteritielis has appeared in commercial poultry flocks, and incidents of 
salmonella poisoning have doubled. 

Until a few years ago, experts believed diat S. enterilidis infected an egg 
through the shell, after the egg was laid, and that frequent egg collection and 
disinfection would minimize contamination. In the 1980s, a new outbreak of 
salmonellosis in the Northeast led to the discovery of salmonella bacteria in 
hens' ovaries, infecting eggs before they were laid. The bacteria have since 
spread to regions outside the Northeast and are becoming antibiotic resistant, 
possibly due to drug overuse by commercial producers. 

An infected hen won't always lay salmonella-contaminated eggs, and a 
hen that usually lays normal eggs may occasionally produce a contaminated 
egg. According to the Centers for Disease Control, only about 1 in 5,000 to 
10,000 eggs is contaminated. The problem is compounded, however, when 
one contaminated egg is added to a recipe along widi several good eggs, or 
foods are served that contain raw eggs. The concentration of bacteria increases 
when egg-rich foods — quiche, homemade eggnog or mayonnaise, custard 
pie, hollandaise and bernaise sauce, and die like — are held at room tempera- 
ture before they are served. 

240 Thl Chicken Health Handbook 

chance of getting salmonellosis from eggs is only about 1 in 2 million. In a 
healthy person, poisoning requires eating a large number of bacteria. Most 
cases occur not in homes but in restaurants, schools, hospitals, and other insti - 
tutions where fresh eggs may not be cooked long enough or may sit on a 
counter too long, allowing any bacteria present to rapidly multiply. Most of the 
500 deaths per year occur in nursing homes. 

Salmonella bacteria, when present, are concentrated in an egg's yolk, 
since the white has antibacterial properties. They may also be present in 
undercooked meat. Although salmonella poisoning from eating chicken gets a 
lot of publicity, rare beef is a more common cause, since most people cook 
their chicken thoroughly. Chicken is thoroughly cooked at 180T (82°C); sal- 
monella bacteria are killed at any temperature above 142'F (61 °C). 

Bacterial Food Poisoning Quick-Check 

Bacteria Incubation Symptoms 

Campylobacter jejuni 2-5 days 

Clostridium botttlimim 1 8-36 hours 

ti-24 hours 

Escherichia coli 

Salmonella spp. 

12-72 hours 

2-8 hours 








no fever 

no fever 

watery or bloody 

no or low fever 



2-7 days 




24 hours 

1-8 days 

2-7 davs 

3-6 hours 

Chickens and Human Health 241 

Many people who have salmonellosis never know it, believing instead that 
they have an upset stomach or a mild case of flu. The illness usually runs its 
course in a week or less. Symptoms begin 1 2 to 72 hours after eating contami- 

abdominal cramps, and diarrhea. 

A serious infection can spread from the intestines to die bloodstream and 
other body sites, causing death, especially among: infants, the elderly, anyone 
with an impaired immune system, a patient undergoing treatment with anti- 
biotics (which remove beneficial bacteria from the intestines, clearing the way 
for disease-causing bacteria), an ulcer patient taking antacids (which reduce 
bacteria-killing stomach acids). 

Most infections are relatively mild and most people recover without treat- 
ment, as long as they avoid dehydration by drinking lots of fluids. 
Hospitalization and antibiotic treatment are needed if symptoms persist 
or the diarrhea is severe and/or accompanied by high fever, weakness, or 

Although campylobacteriosis gets less press than salmonellosis, it is the 
world's leading food-borne pathogen, the most common cause of diarrheal 
illness in humans, and of growing concern to chicken keepers because of its 
prevalence in commercially produced poultry. Of the three species diat cause 
human disease, Campylobacter jejuni — which causes campylobacteriosis in 
chickens — has been identified more than 90 percent of the time. 

Campylobacteriosis is an occupational hazard in poultry processing 
plants. Humans become infected by handling infected birds or by eating 
undercooked infected poultry. (Unlike salmonellosis, campylobacteriosis 
does not infect humans through raw or undercooked eggs.) 

The bacteria produce a toxin that irritates the lining of the intestine, caus- 
ing abdominal pain and watery, sometimes bloody diarrhea, occasionally 
accompanied by a fever ranging from 100" to 104°F (38-40°C). Campylo- 
bacteriosis can be prevented by observing the same precaudons that prevent 
salmonellosis, as outlined on page 242. 

Clostridium Poisoning 

Clostridium perfringensis called die "buffet germ" because it proliferates 
and creates toxins in slowly cooling foods and in foods kept at low holding 
temperatures. Prevent it by keeping cooked meat and eggs at 140° F (60°C) or 
by cooling them quickly to less than 40°F (5"C). When you cook for a crowd, 
divide large amounts of food to speed cooling. Separate chicken from gravy or 
stuffingbefore you store them in the refrigerator. Most strains of C. perfringens 
cause a mild, self-limiting illness, but some can be serious to fatal. See a doctor 

242 The Chicken Health Handbook 

Cooking Poultry 

Follow these precautions whenever you handle poultry meat and eggs. 
Handling Poultry 

When you butcher chickens, avoid feather and fecal contamination; rinse 

meat thoroughly in clear water. 
Thaw frozen poultry thoroughly before cooking it. 
Thaw raw meat in the refrigerator (or in a plastic bag under cold running 

water), never on the counter top. 
Wash hands : knife, cutting board, and other utensils after contact with raw 


Sanitize counters by wiping them with 2 teaspoons of chlorine bleach in a 

quart of warm water. 
Wipe counters with eidier paper towels or a dish cloth washed in soap and 

chlorine bleach after each use. 
Don't let cooked meat (such as chicken barbecue) come into contact with 

raw meat or the plate it was carried on. 

Cooking Poultry 

Heat poultry meat to 185"F (85"C). 
Reheat leftovers to 165"F (74'C). 

Cook casseroles and other combination foods to 1 60 "F (71"C). 
Barbecue until no red shows at the joints. 

Hold cooked poultry above 140°F (60"C) for no longer than 2 hours. 
Handling Eggs 

Collect eggs often and refrigerate them prompdy. 
Don't use cracked or dirty eggs. 
Wash hands and utensils after contac 
Don't serve foods containing uncooked eggs. 


Heat eggs and egg-rich foods to 160"F (71"C). 
Poach eggs for 5 minutes in boiling water. 
Boil eggs in shells for 7 minutes. 

Fry eggs (in an electric frying pan set at 250"F, 121'C) as follows: 
Scrambled, 1 minute; 
Sunnyside up, uncovered, 7 minutes; 
Sunnyside, covered or basted, 4 minutes; 
Over easy. 3 minutes one side, then 2 minutes. 

* and 1 

When in Doubt: Call the toll-free USDA meat and poultry hodine: 


if you experience cramps, severe diarrhea, and bloating gas. 

Clostridium botulimim is usually associated with improperly canned low- 
acid foods. Home-canned vegetables are the most common source, but 
unconfirmed reports have implicated canned chicken meat. Botulinum-laden 
food may or may not appear cloudy, contents may swell causing jars to crack 
or lids to become loose. Do not use any canned food that smells improper or 

ing them. Cook home-canned chicken to 176"F (80°C) for at least 30 minutes 
— the toxin is readily destroyed by heal. 

The botulinum toxin affects the nervous system, causing double vision, 
slurred speech, and difficulty breathing and swallowing. Symptoms may occur 
any rime from 4 hours to 8 days after eating poisoned food, but usually appear 
within 18 to 36 hours. Botulism affects everyone who shares a poisoned meal. 
If you suspect botulism poisoning, get immediate medical attention. Nerve 
damage is irreversible. Untreated botulism poisoning can cause death due to 
paralysis of the respiratory system. 


E. coli from poulU7 droppings may contaminate meat during butchering, 
although avian strains are not a significant cause of infection in humans. Of the 
3 percent of commercial meat contaminated with E. coli, beef is more likely 
than chicken to carry it. Coliform bacteria invade the intestine wall and also 
produce toxins, causing severe cramps and watery diarrhea that soon turns 
bloody. Prevention and treatment is the same as for salmonellosis. 

Staphylococcal Food Poisoning 

Staphylococcus aureus bacteria are present wherever there are chickens. 
About 50 percent of the strains generate toxins that cause food poisoning in 
mishandled poultry meat. Symptoms are nausea, vomiting, cramps, diarrhea, 
and sometimes headache, fever, and prostration. Recovery is usually sponta- 
neous and occurs in about a day. Typically, several people get ill after sharing a 
meal together. Staph bacteria can't be destroyed by heat, making sanitary 
butchering especially important. 

Humans can potentially get a superficial staph infection (impetigo) while 
treating chickens for bumblefoot or an infected breast blister. Although there 
has never been a proven case of a chicken infecting a person, wear plastic 
gloves during treatment and thoroughly wash your hands afterward. 


Diseases and Disorders 

This alphabetic listing is designed to serve as a quick reference to the most critical 
information surrounding common diseases and disorders. The information is 
organized and cross-referenced for easy retrieval Unless otherwise noted, cross 
references are found within this chapter. Following are explanations of the categories 
used in each disease and disorder entry. 

Also Called — alternative names, scientific names (lor the benefit of speciaJists 
and readers who consult teclinical works), and names no longer in vogue (for 
readers who peruse old poultry books) 

Incidence — how common the disease is and the geographic area in which it is 
likely to be found 

System/Organ Aefected — primary body pan or system the disease affects 
Incubation Period — amount of time from exposure to the first sign of infection 

(helps diagnose the disease based on past contacts or identify the source of 

infection once the disease has been diagnosed) 
Progression — how hard the disease hits a flock, how fast it spreads, and whether 

it is acute (short-term, ending in recovery or death) or chronic (long-term) 
Symptoms — most likely symptoms or combinations of symptoms; since no two 

cases are ever exactly alike, not all symptoms will always appear; age groups 

are approximations only 
Percentage Affected — proportion of an affected flock likely to be involved 
Mortality — percentage of affected birds likely to die from the disease 
Postmortem Findings — changes that occur within a diseased bird's body (for 

details on postmortem examination, see chapter 10) 
Resembles — diseases with similar symptoms and, when possible, how to tell 

them apart 

Diagnosis — best way to identify the disease through a combination of flock 
history, symptoms, and postmortem findings; some diseases are so similar to 
others that laboratory tests are required for a positive diagnosis, some can only 
be identified by laboratory tests (for diagnostic guidelines, see chapter 9) 

Cause — primary cause of die disease (for information on the causes of infectious 
diseases, see chapter 7) 

Transmission — how the disease spreads 

Prevention — steps for preventing the disease (for information on immunity, see 
chapter 12) 

TREATMENT — approaches toward dealing with the diseases (for information on 
therapy, see chapter 11) 

Human Health Risk — any potential risk this disease poses for humans (addi- 
tional information can be found in chapter 14) 


A-avitaminosis 245 

- A - 

A-avitaminosis. See Roup (nutrilional) 
Acariasis. See "Mites," page 67 

Acute Death Syndrome. See Sudden Death Syndrome 
Acute Heart Failure. See Sudden Death Syndrome 
Adenoviral Infection. See Infectious Anemia 
AE. See Epidemic Tremor 

Also Called — aspergillus toxicosis, x disease 

Incidence — rare but increasingly more common worldwide 

System/Organ AFFECTED — entire body 

Inciiration Period — up to 2 weeks, depending on amount of toxin ingested 
PROGRESSION — usually acute, sometimes chronic 

Symptoms — in incubated eggs from poisoned hens: embryo death during first 

— in young birds: loss of appetite, slow growth, weakness, increased 
susceptibility to bruising and beat stress, sudden death 

— in hens: reduced egg production, smaller eggs with decreased hatchabil- 
ity, increased susceptibility to infection (especially cecal coccidiosis and 
Marek's disease) 

— in cocks: weight loss, reduced fertility 

Percentage Affected — 100 percent of those consuming contaminated feed 
Mortality — none in aduli chickens 

Postmortem Findings — none or light-colored muscles; sometimes swollen 

kidneys and enlarged liver witii pale yellowish areas that are white at the center 

Resembles — fatty liver syndrome, lymphoid leukosis: infectious anemia, except 
that infectious anemia affects only growing birds 

Diagnosis — difficult: symptoms, feed analysis, microscopic examination of liver 

Cause — toxins produced by Aspergillus flcwus. A. parasiticus, and Penicillium 
puberuluin mold in litter and in corn and other grain (especially grain that's 
insect damaged, drought stressed, or broken into pieces); increases suscepti- 
bility to infectious diseases and often found in combination with infectious 
anemia and /or fatly liver syndrome 

Transmission — eating moldy grain 

Prevention — avoid moldy grain; use only fresh feed (most commercial feeds 
contain mold inhibitors); store feed in plastic bin (metal sweats) in cool, dry 

Treatment — remove and deeply bury moldy grain: minimize stress; boost dietary 
energy and protein and offer a vitamin supplement until recovery 

Human Health Risk — afia toxin (a poison and a carcinogen) is rapidly excreted in 
droppings so there is little danger of residue in meat; residue may appear in 
yolks of eggs up to 10 days after contaminated rations are withdrawn; humans 
may get food poisoning from eating moldy grain 
AI. See Influenza 

Airsacculitis. See Air-Sac Disease 

Air-Sac Disease 

Also Called — airsacculitis. air-sac infection, air-sac syndrome (one form of 

colibacillosis and/or mycoplasmosis) 
Incidence — common worldwide 
System/Organ Affected — respiratory 
Incubation Period — 6 to 21 days 
Progression — acute to chronic 

Symptoms — in young birds, 5 to 1 2 weeks old (most commonly 6 to 9 weeks old): 
coughing, rattling, nasal discharge, breathing difficulty, loss of appetite, rapid 
weight loss, standing around with eyes closed, stunted growth 

Percentage Affected — 100 percent 

Mortality — up to 30 percent 

Postmortem Findings — thick mucus in nasal passages and throat; cloudy air sacs 
containing cheesy material; transparent film covering liver and heart 

Resembles — chronic respiratory disease, except that CRD affects older birds and 
is usually milder 

Diagnosis — flock history, symptoms, postmortem findings, confirmed by 

laboratory identification of bacteria 
Cause — Escherichia coli and Mycoplasma gallisepticum (sometimes M. synoviae) 

bacteria; often occurs in combination with or following vaccination for chronic 

respiratory disease, infectious bronchitis, infectious laryngotracheitis, 


Transmission — contact with infected or carrier birds; inhaling contaminated dust 
or respiratory droplets; spread from breeders to chicks through hatching eggs 

Prevention — avoid dusty litter; provide good ventilation; avoid chilling and other 
forms of stress; buy mycoplasma-f'ree birds 

Treatment — keep birds warm and well fed with high protein rations and a 

vitamin E supplement; treatment with antibiotics such as tylosin (trade name 
Tylan) or eiythromycin (trade name Gallimycin) is effective (/started early and 
bacteria are identified so ineffective drugs can be avoided, otherwise results 
may be variable and disappointing; survivors continue to cany and transmit 
M. gallisepticum 

Human Health Risk — none known 
Algae Poisoning 

Incidence — West and Midwest, rare in chickens 

System /Organ Affected — nervous system or liver and other internal organs 
Incubation Period— minutes 
Progression — acute 

SYMPTOMS — to all ages: weakness, staggering, collapse, convulsions, lying on 
breast with legs extended toward rear, neck extended and curved backward 
until head almost touches back, paralysis, rapid death 

Percentage Affected — 100 percent of those drinking toxic water 

Mortality — 100 percent 

Postmortem Findings — swollen liver 

Resembles — botulism 

Arizonosis 247 

Diagnosis — identification of toxins in water (turns dark green, bluish green, or 
brownish green) 

Cause — two different kinds of toxins in "bloom" or "waterbloom" produced by 
blue green algae (cyanobacteria) growing in shallow inland lakes, ponds, or 
sloughs in warm (72-80"F, 22-27T), dry, low-wind days of summer and fall 
Transmission — drinking surface water containing concentrated toxins 
Prevention — keep chickens away from shallow inland water; apply 3/4 pound 
(12 ounces) copper sulfate (powdered bluestone) per acre of water as bloom is 
forming, repeat every 2 to 3 weeks throughout bloom season 
Treatment — restrict birds' activity; offer vitamin-electrolyte supplement 
Human Health Risk — none 
Ammonia Blindness. SeeConjunctivitis 
Anaphylactic Shock. See "Antibiotic Reactions," page 190. 
Aplastic Anemia. See Infectious Anemia 
Arizona Infection. See Arizonosis 

Also Called — avian arizonosis, AA, Arizona infection, paracolon (one form of 

Incidence — worldwide but rare in chickens 
System/Organ Affected — digestive 
Incubation Period — 5 days 

Progression — acute in chicks, chronic in mature birds 

Symptoms — in chicks up to 3 weeks old: droopiness, closed eyes, diarrhea with 

vent pasting, weakness, twisted neck, resting on hocks, difficulty walking, leg 

paralysis, blindness; sometimes trembling 
Percentage Affected — 100 percent 
Mortality — up to 50 percent, starting at 1 week of age 
Postmortem Findings — retained yolk sac; yellowish, mottled, swollen liver; 

discolored heart; ceca or abdominal cavity filled with cheesy material 
Resembles — paratyphoid; nervous symptoms resemble those of Newcastle and 

other nerve diseases 
Diagnosis — laboratory identification of bacteria 

Cause — Salmonella arizonae bacteria that persist in the environment for months 
and affect turkey poults more often than chicks 

Transmission — contaminated droppings in soil, liner, feed, or water; contami- 
nated feathers, dust, hatchery fluff; spread horn infected breeders to chicks 
through hatching eggs (eggs can blow up during incubation, further spreading 
bacteria); spread by infected eggs and chicks in incubator and brooder; spread 
on dirty equipment, boots, feet of insects and rodents, droppings of infected 
reptiles (especially lizards), rodents, and other animals 

Prevention — keep breeders on wire flooring; collect hatching eggs often; hatch 
only eggs from S. arizonae-bee breeders; hatch only clean eggs; clean and 
disinfect incubator and brooder after each hatch; in chicks, minimize chilling, 
overheating, parasitism, withholding of water or feed; keep water free of 
droppings; control reptiles, rodents, cockroaches, beetles, fleas, and Hies 


Treatment — none effective, survivors are carriers 

Human Health Risk — diarrhea may result from lack of sanitation after handling 
infected chicks 
Arthritis, Staphylococcic. See Staphylococcic Arthritis 
Arthrilis/synovitis. See Staphylococcic Arthritis 
Arthritis, Viral. See Viral Arthritis 
Ascaridiasis. See "Large Roundworm," page 83 
Ascites. See Broiler Ascites 

Asiatic Newcastle Disease. See Newcastle Disease (exotic) 
Aspergillosis (acute) 

Atso Called — Aspergillus infection, brooder pneumonia, mycotic pneumonia, 

pneumomycosis, pulmonary aspergillosis 
INCIDENCE — worldwide but rare 

System/Organ Affected — respiratory; sometimes liver or brain 
Incubation Period — up to 2 weeks 
Progression — acute 

Symptoms — in hatching eggs: green appearance when candled 

— in chicks, usually under 3 weeks of age: gasping, sleepiness, swollen eyes, 

yellow cheesy material in eye, loss of appetite; sometimes nasal discharge, 

diarrhea, twisted neck, paralysis; convulsions, death 
Percentage Afpected — high 
Mortality— up to 10 percent 
Postmortem Findings — grayish yellow lungs 

Resembles — dactylariosis; infectious bronchitis, infectious laryngoiracheilis, and 
Newcastle, except thai acute aspergillosis seldom infects chicks over 40 days old 

Diagnosis — flock history, symptoms, postmortem findings 

Cause — spores of Aspergillus fumigatus fungus and other molds commonly 
found in the poultry environment thai multiply readily at normal incubation 
temperature and humidity 

Transmission — through the shells of hatching eggs, spreads in incubator if 
infected eggs break; inhaled from contaminated air. feed, or brooder litter 

Prevention — do not hatch eggs with cracked or poor shells; thoroughly clean and 
disinfect incubator and brooder between hatches; clean and disinfect feeders 
and waterers daily; avoid stress, moldy liner, moldy feed, dusty conditions 

Treatment — none, cull (try thiabendazole at die rate of J mg/lb or 22 mg/kg 
every 12 hours); prevent reinfection by replacing litter and disinfecting 
incubator and brooder with copper sulfate (powdered Milestone) 

Human Health Risk— the same fungus that affects chicks can affect a human 
with reduced resistance; see "Aspergillosis," page 231 
Aspergillosis (chronic) 

pulmonary aspergillosis 
Incidence — worldwide but rare 

System/Organ Affected — respiratory; sometimes liver or brain 
Incubation Period — 2 weeks or more 
Progression — chronic 

Avian Leukosis 249 

Symptoms — in mature birds: gasping, coughing, bluish comb, loss of appetite, 

rapid weight loss 
Percentage AfBECien — lew at a time 

Mortality — few (higher in confined than in free-ranged birds; highest after birds 
have been handled, especially earned by legs) 

Postmortem Findings — numerous small, yellowish or cream-colored pearl- 
shaped cheesy nodules in lungs (nodules turn green and furry in advanced 
stages); circular, yellow, dished-out nodules attached to air sacs in chest and 

Resembles — infectious bronchitis, infectious laryngotracheitis, and Newcastle, 
except that aspergillosis usually does not cause gurgling, rattling, or other 
respiratory sounds 

Diagnosis — flock history, symptoms, postmortem findings 

Cause — spores of Aspergillus fuinigattis fungus and other molds found in the 
environment of all poultry, especially in areas surrounding feeders and 
walerers (appear blue green and can easily be seen while growing); infects 
confined flocks (especially in winter) where stress is high, nutrition is poor, 
immunity has been reduced by another disease, and/or exposure is heavy 
from seriously moldy litter or grain 

Transmission — inhaled from contaminaied air, feed, or litter, particularly where 
temperature and humidity are high 

Prevention — avoid alternating conditions of wet (when fungi multiply) and dry 
(when fungi spread by blowing in dust); avoid stress, damp or moldy litter, 
moldy feed, dusty conditions; periodically move feeders and waterers or place 
diem on platforms; spray litter with copper sulfate (powdered bluestone); 
control humidity and dust by providing good ventilation (opened windows 
work better than fans) 

Treatment — none, cull; control spread of disease by adding '/ 2 teaspoon copper 
sulfate (powdered bluestone) per gallon of drinking water served in a non- 
metal waterer for 5 days; prevent reinfection by cleaning facilities, disinfecting 
with copper sulfate solution (ft teaspoon per gallon of water), and replacing 

Human Health Risk — the same fungus that affects chickens can affect humans 
with reduced resistance; see "Aspergillosis," page 231 
Aspergillus Infection. See Aspergillosis (acute); Aspergillosis (chronic) 
Aspergillus Toxicosis. See Alia toxicosis 
Avian Arizonosis. SceArizonosis 
Avian Chlamydiosis. SeeChlamydiosis 
Avian Cholera. See Cholera (acute), Cholera (chronic) 
Avian Diphtheria. See Infectious Laryngotracheitis 
Avian Distemper. SeeNewcasde Disease 
Avian Encephalomyelitis. See Epidemic Tremor 
Avian Hemorrhagic Septicemia. See Cholera (acute) 
Avian Infectious Bronchitis. See Infectious Bronchitis 
Avian Influenza. See Influenza 

Avian Leukosis. See Lymphoid Leukosis, Marek's Disease. Osteopetrosis 

250 Avian Malaria 

Avian Malaria. See Malaria 

Avian Malignant Edema. See Necrotic Dermatitis 
Avian Monocytosis. See Bluecomb 

Avian Pasteurellosis. SeeCholera (acute), Cholera (chronic) 

Avian Plasmodia. See Malaria 

Avian Pox. See Pox (dry), Pox (wet) 

Avian Tuberculosis. See Tuberculosis 

Avian Vibrionic Hepatitis. See Campylobacteriosis 


Bacillary White Diarrhea. See Pullorum 
Big Liver Disease. See Lymphoid Leukosis 

Also Called — histomoniasis, infectious enterohepatitis 
Incidence— throughout North American but rare in chickens 
System/Organ Affected — ceca and liver 
Incubation Period — 7 to 1 2 days 
Progression — acute or chronic 

Symptoms — in young birds 4 to 6 weeks old: no symptoms or droopmess, 

drowsiness, weakness, ruffled feathers, increased thirst, loss of appetite, weight 
loss, darkened face; sometimes bloody cecal discharge 

Percentage Affected — 25 to 50 percent 

Mortality — limited to exceeding 30 percent, peaks at 1 7 days, subsides by 28th day 
Postmortem Findings — thickened ceca filled with grayish yellow cheesy, some- 
times blood-tinged, material adhering to the lining; sometimes liver mottled 
with circular, dished-out spots, dark at the center and grayish white or 
yellowish green at the rim (differing from spots due to leukosis, mycosis, 
trichomoniasis, and tuberculosis, which are raised and yellowish gray) 
Resembles — cecal coccidiosis, salmonellosis 

Diagnosis — symptoms, postmortem findings (spots on liver), laboratory identi- 
fication of protozoa required when postmortem findings are insignificant 

Cause — Histomonas meleagi ieiis protozoan present wherever poultry occur 
except where soil is dry, loose, and sandy; free-living forms do not live long, 
but may survive for years in cecal worm eggs; tends to affect turkeys more 
often than chickens 

Transmission — eating droppings from infected chickens, earthworms containing 
infective cecal worm eggs, or protozoa attached to flies, sowbugs, grasshoppers, or 
crickets; carried by cecal worms (Heterakis gallinarum); spread by wild birds 

Prevention — easy, with good management and sanitation; worm regularly 
against cecal worms; place feeders and waterers on wire platforms; low-level 
drugs in feed may be the only preventive in contaminated housing (due to 
longevity of infectious cecal worm eggs, range rotation of free-ranged flocks is 

Human Health Risk — none known 

Botulism 251 


Also Called — avian monocytosis, the greens, mud fever, new wheat disease, 
nonspecific infectious enteritis, pullet disease, summer disease, X disease 
Incidence — rare in chickens 
System/Organ Affected — digestive 
INCUBATION Period — unknown 
Progression — spreads extremely slowly 

Symptoms — in pullets approaching maturity: depression, hunching up, loss of 
appetite, weight loss, distended sour-smelling crop, bluish comb, greenish 
watery or pasty bad-smelling diarrhea, dehydration, sunken eyes, shriveled 
shanks, cold-feeling body 

Sbrgbntage Affected — low 

Mortality — up to 50 percent 

Postmortem Findings — white streaks in breast muscles; sometimes yolk in 

abdominal cavity, mucus-filled intestines, dark liver, swollen kidneys 
Resembles — any acute septicemia 
Diagnosis — difficult 

Cause — unknown (chickens are resistant to the coronavirus that causes 

bluecomb in turkeys), possibly a vims combined with stress induced by hot or 
rainy weather, lack of drinking water, lack of shade, or change in feed; some- 
times foUows the feeding of immature oat or wheat grains 

Transmission — unknown 

Prevention — practice good sanitation; breed for resistance 

Treatment — none known, cull; affected birds may respond to molasses flush (see 

page 192) or '/a teaspoon copper sulfate (powdered bluestone) per gallon of 

drinking water served in a non-metal waterer for 2 days 
Human Health Risk — none known 

Also Called — food poisoning, limberneck, toxicoinfection, Western duck sickness 
Incidence —rare 

System/Organ Affected — nerves 

Incubation Period — high dose of toxin produces symptoms within hours, low 

dose takes up to 2 days 
Progression — acute 

Symptoms — in birds of all ages: sudden death or leg weakness and drowsiness 
followed by progressive flaccid (not rigid) paralysis of legs, wings, and neck, 
difficulty swallowing, ruffled, loose feathers (raised hackles on cocks), lying on 
side with outstretched neck and eyes partly closed; sometimes trembling, 
diarrhea; coma and death due to hearl and/or respiratory paralysis 
Percentage Affected — depends on how many eat the toxin 
Mortality — usually less than 100 percent, depending on amount of toxin 

Postmortem Findings — none obvious; sometimes moudi fills with mucus and 
dirt, or crop and intestines contain suspicious organic matter or maggots 

Resembles — castor-bean poisoning (see page 142); tick paralysis (see "Soft Ticks," 
page 73); lameness caused by mild botulism resembles Marek's disease 

252 Breast Blister 

(pseudo-botulism form), except that in pseudo-botulism birds recover quickly, 
usually within 24 hours 

Diagnosis — flock history (birds ate rotted organic matter), symptoms (progres- 
sive flaccid paralysis, loose feathers, mucus and din in mouth), absence of 
postmortem findings, laboratory identification of bacteria (if Marek's disease 
Or castor-bean poisoning is suspected) 

CAUSE — Clostridium batiilinitm, soil-borne bacteria commonly found in die 
poultry environment that produce toxins when they multiply in warm, moist, 
decaying vegetable or animal matter (including dead chickens) 

Transmission — consuming decayed organic matter, maggots feeding on rotting 
animal tissue, or beedes (in litter) diat contain toxin; drinking water containing 
contaminated organic matter 

PREVENTION — do not feed spoilt 1 food to chickens; burn or deeply bury dead 
rodents, chickens, or other animal carcasses, and rolling, solid vegetables such 
as cabbages; control flies; acidify soil with ammonium sulfate fertilizer; avoid 
wet spots in litter; keep birds away from marshy or swampy areas where 
vegetation rots in water; keep chickens from scratching in compost piles; 
immunize flock widi type C toxoid 

Treatment— remove source of poisoning from yard; move bird to cool environ- 
ment; squirt cool water into crop twice daily; flush with molasses or Epsom 
salts (see "Flushes," page 192); inject intravenously with antitoxin (expensive, if 
available); remove contaminated litter and disinfect widi calcium hypochlorite 
or iodine-based disinfectant 

Human Risk — humans are poisoned by toxin types A, B, E, and I-'; 
chickens are poisoned by type C, rarely by types A and E; chickens and 
humans can be poisoned by the same contaminated food or water; reports of 
human poisoning from eating contaminated chicken meat are unconfirmed 
(see "Clostridium Poisoning," page 241) 
Breast Blister 

Also Called — keel cyst, keel bursitis, sternal bursitis 

Incidence — common 

System/Organ affected — keel 

Progression — chronic 

Symptoms — in growing or mature cocks, particularly of the heavy breeds: large 

blister on keel that eventually becomes a callus or thick scar 
Percentage Affected — up to 10 percent 
Mortality — low 

Resembles — infectious synovitis, except an uninfected blister is filled with clear 

or bloody fluid, an infected blister contains creamy or cheesy material 
Diagnosis — flock history (breed and sex), symptoms 

Cause — irritation and inflammation due to pressure of breast bone against roost 
or wire floor 

Transmission — not contagious; occurs in birds with weak legs or with poor 
feather development offering no breast protecrion; most likely where floor is 
wire, roosts have sharp corners, or litter is wet or hard-packed 

Broiler Ascites 253 

Breast blister 

Prevention — wrap roosts in something soft to cushion the breast bone or do not 

provide a roost for cocks 
Treatmeni' — open and drain blister, clean with iodine, and pack with Neosporin; 

antibiotic treatment in drinking water or by injection may be necessary if 

blister becomes infected with Mycoplasma synoviae (infectious synovitis) or 

Staphylococcus aureus (necrotic dermatitis) 
Human Health Risk — none, as long as blister is not infected 
Broiler Ascites 

Also Called — ascites with right ventral failure, ARVF, dropsy, water belly 
Incidence — common worldwide, especially in winter at high altitudes 
System/Organ Affected — heart 
Incubation Period — unknown 
Progression — acute 

Symptoms — in male broilers 4 to 7 weeks old: ruffled feathers, slow growth, 

reluctance to move; sometimes sudden death 
Percentage Affected — low 
Mortality — up to 30 percent 

Postmortem Findings — dark red muscles; thick, straw-colored fluid in abdominal 
cavity; liver swollen, discolored, and sometimes mottled or pimpled (early 
stage) or small and pale with rounded edges (later stage); bloody lungs; 
distended right side of heart 

Resembles — salt poisoning (see page 31 ) 

Diagnosis — symptoms, postmortem Findings 

Cause — unknown, may be due to genetically inadequate respiratory system 
failing to draw in enough oxygen; may be nutritionally related (e.g., excess salt 
in rations); in newly hatched chicks, may be caused by putting chicks into 
brooder too soon after using volatile disinfectant 

Transmission — unknown 

Prevention — none known; may help to provide good air circulation and avoid 

ammonia fumes 
Treatment — none known 
Human Health Risk — none known 

254 Broiler Runting Syndrome 

Broiler Runting Syndrome. See Infectious Stunting Syndrome 
Bronchitis. See Infectious Bronchitis 

Brooder Pneumonia. See Aspergillosis (acute); Aspergillosis (chronic) 

Also Caixed — staphylococcosis, plantar pododermatitis 
Incidence — common 
System/Organ Affected — foot pad 
Progression — chronic 

Symptoms — in maturing birds, especially in males of heavy breeds: lameness, 
reluctance to walk, inflamed foot (one or both), hot, hard, swollen, or pus-filled 
abscess or dark black scab on bottom of foot, resting on hocks; sometimes 
sores appear on hocks and bottoms of toes 

PERCENTAGE Affected — 1 to 2 percent 

Mortality — usually low; up to 50 percent if untreated 

Postmortem Findings — pus or cheesy material in foot pad; sometimes hock 
joints filled with grayish white fluid 

Diagnosis — symptoms (abscess in foot pad) 

Cause — Staphylococcus aureus bacteria, present wherever there are chickens 

Transmission — coniaminated hatching eggs; bacteria enters fool through injury 
caused by splinters, sharp roosts, jumping from roost on to hard or rocky 
ground, housing on wire, irritation due to improper litter management 

Prevention — practice good sanitation; provide deep, dry litter that does not 
pack; avoid high perches; round off edges of perch and sand off splinters; feed 
vitamin supplement (especially vitamin A); do not breed susceptible chickens 
to avoid getting more of the same 

Treatment — difficult to cure; inject swollen area with S& cc penicillin/streptomy- 
cin (Combiotic); if abscess is large, wash foot, cut open abscess, squeeze out 
cheesy core, rinse well with hydrogen peroxide, pack with Neosporin, wrap 
foot with gauze bandage or strip of clean cloth, and tape; confine bird on deep 
litter and dress foot every 2 or 3 days 

Human Health Risk — superficial skin infection (impetigo); wear plasiic gloves 
when treating a bird, wash hands afterward, gather blister contents in paper 
towel and dispose by burning or deep burial 

Healthy foot (left) compared to 
buinblefoot (right). 

Campylobacteriosis 255 


Cage Fatigue 

Also Called — cage layer fatigue, cage layer osteoporosis, cage layer paralysis, 

INCIDENCE — no longer common 
System/Organ AFFECTED — bones 
Progression — usually chronic but can be acute 

SYMPTOMS — in caged pullets, usually high-production commercial strains in 
summer: weakness, squatting, inability to stand (but will continue to eat and 
drink f feed and water are within reach) 

— in laying hens: thin-shelled eggs with low hatchability followed by 
cessation of laying, paralysis, death due to dehydration 

Percentage Affected — depends on duration of dietary deficiency 

Mortali ty — depends on duration of dietary deficiency 

Postmortem Findings — deformed or collapsed rib cage; soft, thin, or fragile 

bones that break easily 
Resembles — Marek's disease and other paralytic conditions; rickets 
Diagnosis — flock history (age, sex, and housing method), symptoms, postmor- 
tem findings 

Cause — low calcium or phosphorus diet or disturbance in the metabolism of 
dietary minerals, particularly calcium (causing hen to draw calcium from her 
own bones) 

Transmission — nutritional, does not spread from bird lo bird 

Prevention — house hens on litter; feed properly balanced diet supplemented 

wilh ground oyster shell or limestone; allow birds out into the sunshine 
Treatment — calcium phosphate supplement; if hen can't gel up, give 1 gram 

calcium carbonate in a gelatin capsule daily for 1 week, cover wire cage bottom 

with solid boards or move pullets to floor, pullets should recover within a week 
Human Health Risk — none 
Cage Layer Fatigue/Osteoporosis/Paralysis. See Cage Fatigue 

Also Called — avian vibrionic hepatitis, Campylobacter hepatitis, enteric 

campylobacteriosis, infectious hepatitis, liver disease 
Incidence — common worldwide, especially in floor-reared flocks 
System/Organ Aeeected — intestines 
Incubation Period — 24 hours 

Progression — sometimes acute, usually chronic, spreads slowly 
Symptoms — in chicks up to 4 weeks old: depression, watery diarrhea, slow growth 
(chronic), death (acute) 

— in growing or mature birds: sudden death of apparently healthy birds 
(acute) or listlessness, scaly shrunken comb, weight loss, unthriftiness, 
sometimes mucousy. bloody diarrhea (chronic) 

— in hens: 35 percent drop in egg production (may be only sign) 
Percentage Affected — few at a time totaling 30 to 1 00 percent 
Mortality — io to is percent 

POSTMORTEM Findings — intestine filled with mucus and water,' fluid; pale, watery 

256 Candidiasis 

bone marrow; sometimes green- or brown-stained liver with characteristic 
yellow star-shaped patches 

Resembles — blackhead, bluecomb, infectious anemia, cholera, typhoid, lym- 
phoid leukosis, pullorum, ulcerative enteritis 

Diagnosis — symptoms (thin birds), postmortem findings (stars on liver, when 
present), laboratory fecal examination to identify bacteria (since 
Campylobacters are sensitive to drying, ask veterinarian or pathologist for a 
suitable collection container) 

Cause — Campylobacter fetus jejuni bacteria that among birds affect only 
chickens, survive well in the environment, and resist disinfectants; often 
occurs in combination with another infection such as Marek's disease, pox, or 

Transmission — droppings of infected or carrier birds in feed or water; spread by 
flies, cockroaches, and rodents; spread on contaminated equipment and soles 
of shoes; may spread from breeders to chicks through hatching eggs 

Prevention — good management and sanitation; do not combine birds from 
different sources; keep birds free of internal parasites, coccidia, and other 
stress-inducing infections; house chickens on wire to keep them from picking 
in droppings; control flies, cockroaches, rodents; cull weak, unthrifty birds; 
remove infected flock disinfect, and leave housing vacant for 4 weeks before 
introducing new birds 

Treatment — none effective 

Human Heal™ Risk — eating undercooked meat of infected birds can cause 
serious diarrhea, see "Campylobacteriosis," page 241 
Candidiasis. See Thrush 

Also Called — roup, trichomoniasis 

Incidence — worldwide, especially in warm climates or during warm weather, bul 

rare in chickens 
System/Organ Affected — mouth, throat, and crop 
Incubation Period — 2 weeks 
Progression — acute or chronic 

Symptoms — usually in young or growing birds: loss of appetite, rapid weight loss, 
weakness, darkened head, extended neck, frequent swallowing, sunken breast 
(due to empty crop), watery eyes, foul-smelling discharge from mouth, white 
or yellow sores in mouth and throat, inability to close mouth or swallow due to 
massive sores 

Percentage Affected — high 

Mortality — limited, usually within 8 to 10 days due to suffocation 
Postmortem Findings — cheesy white or yellowish raised buttons on throat walls; 

sometimes crop filled with foul-smelling fluid 
Resembles — capillary worms (see page 84), thrush, pox (wet) 
Diagnosis — flock history (drinking from stagnant water), symptoms, laboratory 

identification of protozoa from throat scrapings 
Cause — Trichomonas gallinae protozoan parasite that infects a variety of birds, 

primarily pigeons 

Chlamydiosis 257 

Transmission — stagnant drinking water or feed contaminated with discharge 

from infected bird's mouth; spread by wild birds and pigeons 
Prevention — good sanitation; keep pigeons away from chickens; avoid bringing 

in new birds that may be carriers 
Treatment — move unaffected birds to sanitary surroundings; isolate infected 
birds; combine 1 pound copper sulfate (powdered bluestone) with 1 cup 
vinegar and 1 gallon water, mixwelJ, add 1 tablespoon (V* ounce) solution per 
gallon drinking water for 4 to 7 days, served in a non-metal waterer; non-meat 
birds may be treated with metronidazole (trade name Flagyl) injections or pills 
or with carnidazole (SpartrLx) pills for 5 days; recovered birds are carriers 
Human Health Risk — none known; not the same as trichomoniasis in humans 
Cannibalism. Seepage 135 
Capillariasis. See "Capillary Worm," page 84 
Cauliflower Gut. See Necrotic Enteritis 
Cestodiasis. See "Tapeworm, " page 89 
Chicken Anemia Agent Infection, See Infectious Anemia 
Chicken Pox. See Pox (dry) 

Also Called — avian chlamydiosis, AC. ornithosis, parrot fever, psittacosis 

Incidence — worldwide but rare in chickens 

System/Organ Affected — respiratory, entire body 

Incubation Period — 5 to 9 days 

Progression — acute or chronic, spreads slowly 

charge, greenish yellow diarrhea, loss of appetite, weakness, weight loss 
Percentage Affected — 1 00 percent 
Mortality — mostly in younger birds 

POSTMORTEM Findings — not always obvious; enlarged Q no( { . . . 

discolored liver; dark, soft, enlarged spleen; ' , 

you suspect have 

, cholera, colibacillosis, chlamydiosis 
influenza, mycoplasmosis, pasteurellosis 
Diagnosis — history (contact with infected birds), symptoms, postmortem 

findings, laboratory identification of chlamydia 
G\use — Chlamydia psittaci, a bacteria-like organism that affects many species of 
bird but cannot survive long offbirds; often found in combination with 

Transmission — contagious; contact with infected birds and their droppings or 

inhaled dust; spread by wild birds 
Prevention — control wild birds; blood test periodically and cull reactors where 

outbreaks occur; keep chickens away from ponds, lakes, and other surface 

water frequented by wild birds; after an outbreak, disinfect with quaternary 

ammonium compound or an alcohol-iodine solution 
Treatment — none effective, relapse is likely, survivors may be carriers; this is a 

reportable disease, see "Reportable Diseases" page 196 
Human Health Risk — high chance of lung infection, see "Chlamydiosis," page 235 

258 Cholera (acute) 

Cholera (acute) 

Also Called — avian cholera, avian hemorrhagic septicemia, avian pasteurellosis, 
fowl cholera 

Incidence — relatively common worldwide; more likely in warm climates and in 

free-ranged birds; more prevalent in late summer, fall, and winter 
System/Organ Affected — entire body (septicemic) 
Incubation Period— 4 to 9 days 
Progression — acute, spreads rapidly, kills quickly 

Symptoms — in mature birds or those approaching maturity: sudden death (hens 
dead in nests) or fever, loss of appetite, increased thirst, depression, drowsi- 
ness, ruffled feathers, head pale and drawn back, increased respiratory rate, 
mucous discharge from mouth and nose, watery white diarrhea later becom- 
ing thick and greenish yellow, bluish comb and wattles, death within hours of 
first symptoms; survivors may recover and either eventually die from emacia- 
tion and dehydration or develop chronic cholera 

Percentage Affected — high 

Mortality — 10 to 20 percent among mature birds, can be as high as 45 percent; 
rare in birds under 1 6 weeks old 

Postmortem Findings — none in case of sudden death, otherwise blood in lungs 
and in fatty tissue of abdomen; heart surrounded by fluid containing cheesy 
flakes; swollen, grayish liver (looks cooked) with small grayish while spots 
(resembles cornmeal); sticky mucus in digestive tract, especially in the crop 
and intestine 

— in hens: yolk in abdominal cavity 

Resembles — erysipelas, septicemic colibacillosis, poisoning (see page 139), 

Diagnosis — symptoms, postmortem findings, laboratory identification of 

Cause— Pasteiirella multocida bacteria that affect a variety of birds and increase 
in virulence as disease spreads; bacteria survive for 1 month in manure, 3 
months in moist soil; destroyed in 10 minutes by sunlight, also easily destroyed 
by disinfectants, drying, heat 

Transmission — contagious; contact with mucus from the nose, mouth, or eyes of 
birds or animals with chronic infection; mucus contaminating feed or drinking 
water; mucus on feed sacks, shoes, and used equipment; picking at carcasses 
of dead birds 

Prevention — vaccination is not effective; purchase only cholera-free birds; avoid 
purchasing growing or mature birds, which may be carriers; avoid stress due to 
heat, rough handling, parasites, abrupt change in rations, poor nutrition, and 
poor sanitation; provide clean, safe drinking water; do not mix birds of 
different ages; control wild birds, rodents, and other animals; keep pets away 
from chickens; burn or deeply bury carcasses of dead chickens 

Treatment — none effective, disease recurs when medication is discontinued and 
survivors maybe carriers; isolate and dispose of infected flock, thoroughly 
disinfect and dry housing, leave it vacant at least 3 months before introducing 
new birds 

Cholera (chronic) 259 

Human Health Risk — in poorly ventilated housing, possible upper respiratory 
tract infection (which can in turn infect chickens through mucus discharged 
from human's mouth or nose); wear protective mask 
Cholera (chronic) 

Also Called — avian cholera, avian pasleurellosis, endemic fowl cholera, roup 

Incidence — worldwide but less common than acute cholera 

System/Organ Affected — primarily respiratory 

Incubation Period — weeks to months 

Progression — chronic 

Symptoms — in birds at least 6 weeks old: cheesy nasal discharge, loss of appetite, 
rapid weight loss, increased thirst; lameness or swelling of leg joints, wing 
joints, foot pads, wattles, and sinuses; swollen, sticky eyes; sometimes bluish, 
hot comb; sometimes breathing difficulties, rattling, and sneezing 

— in hens: crop in egg production, increased blood spotting in eggs 

— in cocks: loss of aggressive behavior and desire to crow 
Percentage AFFECTED — limited 

Mortality — limited 

Postmortem Findings — sinuses filled with yellow cheesy material; white cheesy 

matter along breast bone; wrinkled, bloody and/or off-colored yolks 
Resembles — bluecomb, which is even less common than chronic cholera; 

infectious coryza. except that coryza is associated with a foul odor; Newcastle, 

except that Newcastle often includes nervous symptoms 
Diagnosis — symptoms, postmortem findings, laboratory identification of 


Cause — Pasteureila muftocida (also called P. septica) bacteria of low virulence or 
lingering after an acute cholera infection 

Transmission — contagious; contact with mucus from the nose, mouth, or eyes of 
carriers, including wild birds, wild animals (opossums, rodents, raccoons), 
domestic animals (dogs, pigs); feed or drinking water contaminated with 
mucus; mucus on feed sacks, shoes, and used equipment; picking at the 
carcasses of dead birds 

Face swollen with 

Prevention — same as for acute cholera 

TREATMENT — same as for acme cholera 

Human Health Risk — same as for acute cholera 
Chondrodystrophy. .See Slipped Tendon 
Chronic Respiratory Disease 

Also Called — CRD, MG, PPLO (pleuropneumonialike organism) infection, stress 
disease (one form of mycoplasmosis) (the same disease in turkeys is called 
"infectious sinusitis") 

Incidence — common worldwide, primarily in winter in large commercial flocks 

SYSTEM/ORGAN Affected — respiratory, sometimes entire body 

Incubation Period— 6 to 21 days 

Progression — chronic, spreads slowly, lasts longer in colder weather 

Symitoms — in broilers. 3 to 8 weeks old: drop in feed consumption, slow growth 
— in growing or mature birds: no symptoms or droopiness, coughing, 
sneezing, rattling, gurgling, swollen face, nasal discharge, ruffled feathers, 
frothy eyes, squeaky crow, drop in laying; sometimes darkened head, loss of 
appetite, weight loss, yellowish droppings 

Percentage Affected — nearly 100 percent 

Mortality — usually low except in young birds 

Postmortem Findings — thick mucus in nasal passages and throat; cheesy 
material in air sacs; thickened heart sac; transparent film covering liver 

Resembles — other respiratory diseases (infectious coryza, cholera, infectious 
bronchitis, Newcastle), except that CRD spreads more slowly than most 

Diagnosis — flock history (time of year, age, potential contact with carriers), 
symptoms (respiratory distress, weight loss, drop in laying), postmortem 
findings, laboratory identification of bacteria 

Cause — Mycoplasma gallisepticuni bacteria, often aided by Escherichia coliaoAl 
or a reovirus; often seen in combination with cholera, infectious bronchitis, 
infectious coryza, Newcastle; often follows vaccination for infectious bronchi- 
tis or Newcastle 

Transmission — contagious; contact with infected or carrier birds and their 
respiratory discharges; inhaling contaminated dust; spread from breeders 
through hatching eggs; spreads on shoes, crates, etc. 

Prevention — purchase mycoplasma-free stock; minimize stress due to sudden 
weather changes, feed changes, drafts, chilling, crowding, transporting, 
showing, worming, vaccinating, dust, and ammonia fumes; vaccinate; after 
outbreak, clean and disinfect housing and leave empty for a few weeks 

Treatment — none effective; tylosin (Tylan) or erythromycin (Gallimycin) will 
reduce death rate but survivors are carriers; this is a reportable disease in 
many states, see "Reportable Diseases" page 196 

Human Health Risk — none known 
Circling Disease. See Listeriosis 
Cloacitis. See Pasted Vent 

, See Necrotic Dermatitis 

Coccidiosis (intestinal) 26 1 

Coccidiosis (cecal) 

Also Called — cocci (coxy) 

Incidence — common worldwide, especially in warm, humid weather 
System/Organ Affected — cecum 
INCUBATION Period — 5 to 6 days 

Progression — usually acute, spreads rapidly, survivors recover in 10 to 14 days 
Symptoms — in chicks or young birds: droopiness, huddling with ruffled feathers. 

loss of appetite, retarded growth, bloody diarrhea in early stages 
Percentage Affected— 80 to 100 percent 
Mortality — high 

POSTMORTEM Findings — pale breast muscles, swollen cecal pouches filled with 

bloody or cheesy material — blackhead, necrotic enteritis, salmonellosis 
Diagnosis — Hock history, postmortem findings, fecal test (see page 92) 
Cause — Eimerio lenella coccidial protozoan parasites 

Transmission — contact with droppings of infected birds; spread on used equip- 
ment, feed sacks, feet of humans and wild birds, etc. 

Prevention — defies good sanitation; breed for resistance; hatch and brood chicks 
early in the season; raise chicks on clean, dry litter to expose them gradually 
and let them develop resistance; avoid crowded, damp conditions; in warm, 
damp weather, treat chicks to 16 weeks of age with medicated starter or 
coccicliostat in drinking water, according to directions on label (excessive use of 
rucckliostat can be toxic); most adults are immune 

Treatment — 1 teaspoon amprolium (20 percent) per gallon drinking water for 5 
days; antibiotic treatment guards against secondary infection; follow treat- 
ment with a vitamin supplement (especially A and K); survivors are immune, 
but may never be as productive as uninfected birds 

Human Health Risk — none known 
Coccidiosis (intestinal) 

Also Called — cocci (coxy) 

Incidence — common worldwide, especially in warm, humid weather 
System/Organ Affected — intestinal tract 
Incubation Period — 5 days 
Progression — usually chronic 

Symptoms — in growing or semi-mature birds: droopiness, huddling with ruffled 
feathers, loss of interest in water and feed, retarded growth or weight loss, 
watery, mucousy, or pasty, tan or blood-u'nged diarrhea (see chart 6-2 page 
1001; sometimes emaciation and dehydration 

— in mature birds: thin breast, weak legs, drop in laying; sometimes 

— in yellow-skinned breeds or all ages: pale comb, skin, and shanks 
Percentage Affect ed — 80 to 100 percent 

Mortality — limited to high 

Postmortem Findings— vary with Eimeria species (see chart 6-2 page 100) 

Resembles — infectious anemia, 
other enteritic diseases 

262 Coccidiosis (respiratory) 

Diagnosis — flock history (exposure to large number of oocysts), symptoms, 
postmortem findings, fecal test (see page 92) 

page 1 00) that flourish in warm, humid environments and survive for long 
periods outside a bird's body; more than one species may infect a bird at one 
time; the presence of coccidia does not always cause infection 

Transmission — droppings of infected birds; spread on used equipment, feed 
sacks, feet of humans and wild birds, etc. 

Prevention — same as for cecal coccidiosis; not all coccidiostats are effective 
against all coccidia! species 

Treatment — same as for cecal coccidiosis (except that choice of drugs depends 
on identification of species involved); survivors are immune to thecoccidial 
species causing the infection, but may not be as productive as uninfected birds 

Human Health Risk — none known 
Coccidiosis (respiratory). SeeCryptosporidiosis 
Cold. See Infectious Coryza, Infectious Bronchitis 

Colibacillosis. (See a/so Air-Sac Disease, Chronic Respiratory Disease, Infectious 
Synovitis, Omphalitis, Swollen Head Disease) 
Also Called — coliform infection, £ coli infection 
Incidence— common worldwide 
System/Organ Affected — various 

Progression — severe and acute to mild and chronic; spreads rapidly 
Symptoms — in incubated eggs: dead embryos late in incubation with watery 

yellowish brown yolk sacs, instead of normal thick yellowish green (yolk sac 


— in newly hatched chicks: swollen, inflamed navel, death within 6 days of 
hatching (omphalitis) 

— in growing birds: lameness, listlessness, ruffled feathers, fever, swollen 
joints, recovery in about a week or emaciation (infectious synovitis) 

— in growing or mature birds: sudden numerous deaths of apparently 
healthy birds with full crops (acute septicemia) 

— in mature birds: clear eye that becomes blind, swollen leg joint filled with 
golden-colored fluid (infectious synovitis), yellow, watery, or foamy diarrhea 

— in hens: cessation of laying, upright penguin-like posture, death within 6 
months (salpingitis) 

Percentage Affected — varies 
Mortality— varies 

Postmortem Findings — vary with location of infection, may include: dehydration; 
greenish liver; swollen liver, spleen, and kidneys with grayish dots; cheesy or 
fibrous material covering heart; thick, inflamed intestines filled with mucus 
and blood 

— in hens: yellowish fluid or yolk-like material in body cavity or distended 
page 53) 

Conjunctivitis 263 

Resembles — many other diseases; acute septicemia resembles cholera and 

Diagnosis — flock history, sympioms, postmortem findings, laboratory identifica- 
tion of bacteria 

Cause — many strains of Escherichia coll bacteria commonly found in the poultry 
envircnment that infect birds with impaired resistance; often occurs as a 
secondary infection to chronic respiratory disease or infectious coryza 

Transmission — ingested droppings of infected birds or mammals in feed or 
water; spread by infected hreeders to chicks through halching eggs 

Prevention — good sanitation and ventilation; avoid stress: keep drinking water 
free of droppings; control rodents; practice good incubator sanitation and 
hatch only clean eggs 

Treatment — keep birds warm and well Ted with high protein rations and a 

vitamin F. supplement; antibiotic treatment is effective only if started early and 
E. co/istrain is identified in order to avoid ineffective drugs, otherwise results 
of treatment can be variable and disappointing 

Human Health Risk — minimal (see "Escherichia Coli", page 243) 
Coliform Infection. SeeColibacillosis 
Congenital Loco. See Congenital Tremor 
Congenital Tremor 

Also Called — congenital loco, jittery chicks, crazy chick disease (not the same as 
encephalomalacia, which is also called crazy chick disease) 

Incidence — rare 

System/Organ Affected — nervous system 

Symptoms — in newly hatched chicks: uncontrolled movements, head tremors, 
sagging of head until beak touches floor, standing only a short time before 
falling over backward (somersaulting), death due to inability to eat or drink 

Percentage Affected — low 

Mortality — 100 percent 

Postmortem Findings — irregularities in muscle, bone, and/orbrain 
Resembles — epidemic tremor and encephalomalacia, except that congenital 

tremor starts at the time of hatch 
Diagnosis — symptoms 

Cause — injury during halching or hereditary defect caused by a recessive genetic 

Transmission — does not spread 
Prevention — cull breeders whose chicks are affected 
Treatment — none; cull 
Human Health Risk — none 

Also Called — ammonia blindness, keratoconjunctivitis 

Incidence — common in flocks raised on deep litter, especially in winter 

System/Organ Affected — eyes 

Incubation Period — hours 

Progression — acute 

264 Contagious Catarrh 

Symptoms — in all ages: rubbing eyes with wings, reluctance to move, avoiding 
sunlight, one or both eyes cloudy (in case of vitamin A deficiency, nose and 
eyes water, later become encrusted with white cheesy material), blindness 

Percentage Affected — 80 to 1 00 percent 

Mortality — varies 

Postmortem Findings — none significant 
Resembles — any mild respiratory disease 

Diagnosis — history (detection of ammonia fumes), symptoms (eye and eyelid 

Cause — ammonia fumes from accumulated droppings, vitamin A deficiency, 

Transmission — environmental, does not spread from bird to bird 
Prevention — provide proper nutrition and good ventilation; avoid wet litter 
Treatment — replacing wet litter or correcting vitamin A deficiency in early stages 

leads to recovery in about 2 months, but won't reverse blindness 
Human HEALTH Risk — squinting in ammonia fumes is no less unpleasant for 
humans than it is for chickens 
Contagious Catarrh. .See Infectious Coryza 
Coryza. .See Infectious Coryza 

Crazy Chick Disease. See Encephalomalacia, Congenital Tremor 
CRD. See Chronic Respiratory Disease 
Crooked Legs. See Twisted Leg 
Crop Binding. See Crop Impaction 
Crop Impaction 

Incidence — rare 
System/Organ Affected — crop 

Symptoms — in mature birds: distended, sour-smelling crop filled with feed and 

roughage (crop feels hard when pressed between fingers), emaciation 
Percentage Affected —up to 5 percent 
Mor tality — limited, deaths due to impaired digestion 
Postmortem Findings — sometimes sores in crop lining 

Resembles — thrush, except that in crop impaction birds appear otherwise healthy 
Diagnosis — symptoms 

Cause — unknown, possibly genetic susceptibility, injury, fungal infection, 

improper fermentation of crop contents, or insufficient rations forcing birds to 
eat litter or fibrous vegetation that pack the crop until it loses muscle tone and 
cannot empty itself 

Transmission — does not spread from bird lo bird 

Prevention — provide proper rations and plenty of clean, fresh water; if feed is 
withheld preparatory to worming, offer a moistened ration 1 hour after 

Treatment — disinfect skin, slit through skin with very sharp blade, pull skin aside 
and slit through crop, clean out crop, isolate bird and keep wound clean until it 

Human Health Risk — none 

Dactylariosis 265 

Crop Mycosis. See Thrush 
Crud. See Necrotic Enteritis 

Also Called — coccidiosis 
Incidence — not common 

System/Okgan AFFECTED — respirators' (lungs, air sacs), cloaca, cloacal bursa 

Progression — acute (lasting 2 to 3 weeks) or chronic 

Symptoms — in birds 4 to 1 7 weeks old: no symptoms or pale skin, coughing, 
sneezing, swollen sinuses, nose and eye discharge, extending neck to breath, 
sitting widi weight on keel, reluctance to move, slow growth; sometimes 

Percentage Affected — 5 to 25 percent 
Mortality — higb 

Postmortem Findings — air sacs contain clear, foamy, white, or gray fluid or thick, 

white, cheesy material; ceca filled widi foamy fluid 
Resembles — any mild respiratory disease 

Diagnosis — laboratory identification of oocysts from moist cotton swab vigor- 
ously rubbed against windpipe 

infected birds 

Prevention — none known other than meticulous sanitation 

Treatment — none known; reduce mortality; with supportive therapy (see page 

192) and treatment of concurreni infection(s); survivors are immune 
Human Health Risk — none known 

Curled-Toe Paralysis. See "Crooked Toes," page 226 

Cutaneous Pox. See Pox (dry) 



Also Called — dactylaria 
Incidence — rare 

System/Organ Affected — brain, lungs 
Incubation Period — 6 to 1 days 
Progression — acute 

Symptoms — in chicks 1 to 6 weeks of age: tremors, circling, incoordination 

Percentage Affected — up to 5 percent 

Mortality — up to 100 percent 

Postmortem Findings — granular tumors in brain 

RESEMBLES — aspergillosis, encephalomalacia 

Diagnosis — flock history (age of birds, litter derived from wood) , symptoms, 

postmortem findings 
Cause — Dactylaria gullopava fungus contaminating sawdust or shredded tree 

bark used as litter 

266 Dikkop 

Transmission — inhaled from moldy litter 

Prevention — avoid moldy litter 

TREATMENT — cull affected birds and replace litter 

Human Health Risk — none known 
Dikkop. .See Swollen Head Syndrome 
Diphtheritic Pox. See Pox (wet ) 
Dermatitis, Necrotic. .Sec Necrotic Dermatitis 
Dermatitis, Vesicular. See Ergotism 
Dropsy. .See Broiler Ascites 

- E - 

Egg Binding. Sec page 54 
Egg Drop Syndrome 

Also Called — EDS 

Incidence — sporadic worldwide, except in North America 

System/Organ Affected — reproductive 

Incubation Period — 7 to 1 7 days 

Progression — spreads slowly, lasts 4 to 1 weeks 

SYMPTOMS — in mature hens, especially broiler-breeders and brown-egg layers: 
gradual drop in laying up to 40 percent lasting 4 to 10 weeks, eggs witii pale 
shells, thin gritty shells, soft shells, or no shells (hens may eat eggs, making it 
look like they are laying less than they actually are) 

Percentage Affected — varies greatly 

Mortality — low 

Postmortem Findings — none obvious; inactive ovary and atrophied oviduct — Newcastle and influenza in loss of egg quality, except that in EDS 

birds do not appear sick; infectious bronchitis, except bronchitis does not 

involve soft-shelled or shell-less eggs 
Diagnosis — symptoms (pale-shelled, thin-shelled, soft-shelled, and shell-less 

eggs Hearing peak of production); laboratory identification of virus through 

blood testing 

Cause — adenovirus (originally introduced into chicken flocks through Marek's 
vaccine grown in a medium derived from duck embryos); the virus is primarily 
carried by ducks and geese but does not infect them 

Transmission — contact with infected waterfowl or surface water contaminated 
by them: spread from breeders to chjeks through hatching eggs; contact with 
infected chickens and their body discharges, especially droppings; contact 
with contaminated equipment, particularly cartons for hatching egg storage 

Prevention — good sanitation; breed for resistance; vaccinate birds at 14 to 16 
weeks of age: avoid flockwide injections or vaccinations using one needle; 
scrupulous sanitation limits the virus's spread 

Treatment — none; discard obviously affected eggs; force molt hens to renew 

Human Health Risk — none known 

Encephalomalacia 267 


Also Called — windpuff 
Incidence — rare 

System/Organ Affected — respiratory 

Symptoms — bird grows large and round without associated weight gain 

Percentage AFFECTED — individual birds 

Mortality — only among severely affected birds 

Postmortem Findings — accumulation of air beneath the skin 

Resembles — no other disease 

Diagnosis — symptoms, postmortem findings 

G\use— ruptured air sac due to a defect in the respiratory tract or injury due to 
rough handling, capon izing, crash landing while flying, heavy coughing caused 
by respiratory infection 

Transmission — unknown; often follows brooder house fires 

Prevention — unknown 

Treatment — release air by puncniring skin wilh a large hypodermic needle or 

other sharp Instrument 
Human Health Risk — none known 

Auso CALLED — crazy chick disease 
Incidence. — rare 
System/Organ Affected — brain 
Progression — acute 

Symptoms — in chicks 1 to 8 weeks (most commonly 2 to 4 weeks) old: sudden loss 
of balance with legs outstretched, toes flexed, head pulled in or bent back, 
flapping wings and falling over, circling, moving head from side to side; 
sometimes trembling head and legs; paralysis, death 

— in hens: 15 to 30 percent drop in laying for up to 2 weeks 

Percentage Affected — 1 to 10 percent 

Mortality — 100 percent in chicks 

Postmortem Findings — none or softened, swollen, deteriorated brain with red, 
brown, or greenish yellow discoloration 

Chick sufferingfroni eiicepluilonidkichi 

Resembles — curled-toe paralysis, except that in curled-toe paralysis loes curl 
instead of flex and chicks tend to walk on their hocks (see "Crooked Toes," 
page 226); pyridoxine deficiency, except that in pyridoxine deficiency the 
nervous activity is much more intense and often ends in death (see "Brooding 
Deficiencies," page 227) 
Diagnosis — symptoms, postmortem findings, ration evaluation 
Cause — vitamin E deficiency, often related to selenium deficiency 
Transmission — nutritional, does not spread from bird to bird 
PREVENTION — use only fresh feed, fortified with vitamin E and containing anti- 
oxidants; store feed in cool dry place, use within 2 weeks of purchase; do not 
use expired vitamin supplements 
Treatment— successful only if begun before brain is seriously damaged; for 
chicks: Vi teaspoon vitamin AD&E powder per gallon of water until symptoms 
disappear; for older birds: V* ccAD&E injected into breast (intramuscular) in 
addition to vitamin powder in drinking water; recovered birds may be blind in 
one or both eyes 
Human Health Risk— none 
Encephalomyelitis. See Epidemic Tremor 
Endemic Fowl Cholera. See Cholera (chronic) 
Endemic Newcastle. See Newcastle Disease 
Enlarged Hock Disease. Sec Infectious Synovitis 
Enteric Campylobacteriosis. SwCampylobacteriosis 

Enteritis. See Bluecomb, Colibacillosis, Infectious Stunting Syndrome, Necrotic 

Enteritis. Roiaviral Enteritis, Ulcerative Enteritis 
Enterohcpatitis. See Blackhead 
Enterotoxemia. See Necrotic Enteritis 
Epidemic Tremor 

Also Called — avian encephalomyelitis, AE, encephalomyelitis, infectious avian 

encephalomyelitis, New England disease, star-gazing syndrome 
Incidence — worldwide but rare; more often in large commercial flocks in winter 

and spring 
System/Organ Ahkec ted — nervous system 
Incubation Period — 5 to 40 days (9 to 21 average) 
Progression — rapid, lasts 21 to 30 days in mature birds 

Symptoms — in 1- to 3-week-old chicks: dull eyes followed by losi coordination, 
jerky or irregular gait, inability to stand, sitting on hocks, falling over with 
outstretched wing, weak peeping; sometimes periodic vibration of the head 
and neck and "buzzing" sound when chick is held; death clue to inability to eal 
or to being trampled by odier chicks 

— in mature hens (symptoms easily go unnoticed): 5 to 10 percent drop in 
egg production for 2 weeks, poor halchability of eggs, poor livability of chicks 

Percentage Affected — 46 to (50 percent 

Mortality — in chicks: 25 percent average, may be as high as 90 percent in 

mature birds: none 
Postmortem Findings — none obvious 

Resembles — congenital tremor, except that congenital tremor affects chicks from 

Chick dead from epidemic iremor 

the time of hatch; encephalomala- 
cia, except that encephalomalacia 
usually affects older chicks; Marek's , ^ , " 
disease, except that Marek's usually 
affects much older birds; Newcastle, 
encephalitis (bacterial, fungal, or 
mycoplasmal), rickets, deficiency of 
riboflavin or vitamin A or E, salt or 
pesticide poisoning (see "Poisoning," 
page 139) 
Diagnosis — history (age of birds), 
symptoms, confirmed by laboratory 

Cause — picornavirus that survives for up to 4 weeks in droppings 
Transmission — contact with infected birds or their droppings; spread from 

infected breeders through hatching eggs; spread by turkeys, pheasants, 

coturnrx quail; spreads on used equipment; spread by licks 
Prevention — cull breeders whose chicks are affected; vaccinate breeder pullets 

over 8 weeks of age, but at least 4 weeks before production starts 
Treatment— none; chicks may survive but should be culled since they will never 

be good layers or breeders; survivors of an adult outbreak become immune 

and are not carriers 
Human HEALTH Risk — none known 

Also Called — sod disease, vesicular dermatitis 
Incidence — worldwide but rare 

System/Organ Affected — endocrine, nervous, blood vessels 

Symptoms — in all ages: listlessness; loss of appetite; increased thirst; diarrhea; 
convulsions; bluish, wilted, cold comb that eventually shrivels; abnormal 
feathering; sores on legs, shanks, and tops of toes; slow growth; low egg 

Percentage affected — low 

Mortality — 25 percent 

Postmortem Findings — inflamed intestines 

Fusarium spp in corn, barley, brewer's grains, oats, sorghum, and safflower 

Diagnosis — flock history (fed moldy grains), symptoms, feed analysis 

Cause — toxic alkaloids produced by purpurea fungus in stored wheat, 

rye, and other cereal grains 
Transmission — contaminated j 
Prevention — use commercially prepared, \ 
Treatment — replace contaminated feed 
Human Health Risk — humans ma 

Also Called — Erysipelodntx infection 

270 Eiysipelothrix Infection 

Incidence — worldwide bin rare in chickens; most likely to occur in cool months 
System/Organ Affected — entire body (septicemic) 
Incubation Period — short 

Progression — acute, sometimes followed by chronic infection 

SYMPTOMS — usually in growing free-ranged cocks: listlessness, loss of appetite, 

difficulties, lameness due to swollen joints, purple blotches on skin; sudden 

- in cocks: reduced fertility 

— in hens: up to 70 percent drop in egg production 
Percentage Affected — up to 40 percent 

Mortality — nearly 1 00 percent 

Postmortem Findings — none significant or small blood spots in almost any lissue 
or organ; swollen liver, kidney, spleen; yellow nodules in ceca; pus surround- 
ing swollen joints 

Resembles — cholera, except that cholera does not cause enlarged spleen; 
chlamydiosis, colibacillosis, Newcastle, salmonellosis, streptococcosis 

Diagnosis — flock history (age and sex, presence of wounds, birds ranged on land 
that once held turkeys, pigs, or sheep), symptoms (sudden losses among 
apparently healthy cockerels), postmortem findings (blood-spotted breast 
muscle), confirmed by laboratory identification of bacteria 

Cause — Eiysipeloihrix rhusiopaihiae bacteria that survives for many years in 
alkaline soil and is resistant to disinfectants; affects turkeys more often than 
chickens; often follows stress due to overcrowding, dampness, bad weather, 
poor sanitation, ration change, vaccination 

Transmission — bacteria in soil from droppings of infected chickens (or turkeys, 
pigs, or sheep) enters through wounds caused by fighting, cannibalism, or 
poorly designed equipment; bacteria ingested from soil, water, or meat 

Prevention — breed for genetic resistance; in erysipelas- prone areas, keep 
chickens away from range previously occupied by turkeys, pigs, or sheep; 
avoid crowding; control rodents 

Treatment — since disease poses human health risk, eliminate infected flock and 
start over on fresh ground; otherwise, move birds to clean environment (will 
control losses but contaminate new ground); add sodium or potassium 
penicillin to drinking water at the rate of 1,000,000 IU per gallon for 5 days; 
survivors are resistant to future infection, but may be carriers 

Human Health Risk — painful infection that can be serious to fatal withoui 
medical attention; see "Erysipeloid," page 236 
Erysipelolhrix Infection. Sep Erysipelas 

Escherichia coli Infections. See Air-Sac Disease, Chronic Respiratory Disease, 

Colibacillosis, Omphalitis, Swollen Head Disease 
European Fowl Pest. See influenza 
Exotic Newcastle Disease. See Newcastle Disease (exotic) 
Exudative Diathesis 

Also Called — exudate diathesis 

Fatly Liver Syndrome 271 

Incidence— rare 

System/Organ AFFECTED — skin and muscle tissue 

Symptoms— in chicks 1 to 4 weeks old: breast and legs look greenish blue, chicks 

stand with legs far apart due to fluid under skin, paralysis 
Percentage Affected — 1 to 5 percent 
Mortality — 100 percent 

Postmortem Findings— yellow or bluish green gelatinous fluid under skin; blood 

spots in breast and leg muscles 
Diagnosis— symptoms, postmortem findings, ration evaluation 
Cause — vitamin E deficiency, usually related to selenium deficiency; sometimes 

occurs in combination with white muscle disease 
Transmission — nutritional problem, does not spread from bird to bird 
Prevention — use only fresh feed fortified with vitamin E and selenium; store feed 

in cool dry place and use within 2 weeks of purchase 
Treatment — vitamin E and selenium supplement in feed or orally (300 IU per 

bird); replace old feed 
Human HEALTH Risk — none 

- F - 

Facial Cellulitis. See Swollen I lead Syndrome 
False Botulism. .See Marek's Disease 
Fatal Syncope. See Sudden Death Syndrome 
Fatty Liver Syndrome 

Also Called — fatty liver and kidney syndrome, FLKS, pink disease 
Incidence — sporadic worldwide 
System/Organ AFFECTED — liver 
Progression — chronic 

Symptoms — in commercial broiler chicks: depression, ruffled feathers, inability to 

— in mature hens, particularly in warm weather: sudden death (sometimes 
after puncture from cock's toenails) or sudden drop in laying to about 50 
percent, diarrhea; someiimes overweight (25 to 35 percent above normal); 
enlarged, pale combs and wattles 
Percentage Affected — ■] to 5 percent, depending on diet 
Mortality — less than 5 percent (dead birds have pale heads) 
Postmortem Findings — excess body fat, often pink; mushy yellow, greasy liver; 
pale, yellowish heart; dark, smelly matter in small intestine; sometimes large 
blood clots in abdomen (called "fatty liver-hemorrhagic syndrome" or "FLHS") 
Resembles — campylobacleriosis 

Diagnosis — flock history, symptoms, postmortem findings 

Cause — unknown; may be genetic; may be caused by molds ir. feed or water that 
damage liver; may be caused by high stress due to beat, high egg production, 
inapparent disease; may be due to biotin deficiency, perhaps caused by 
disease that increases biotin requirement; often associated with high-energy 
feeds combined with inactivity 

Transmission — nutritional, does not spread from bird to bird 

272 Favus 

Prevention — avoid moldy or high-energy feeds (consisting mostly of grains), 
raise birds on litter with room for activity; provide good ventilation to prevent 
heat stress 

Treatment — none effective; restrict feed consumption; substitute wheat bran for 
part of corn; feed brewer's yeast, dried molasses, or alfalfa and other green 
leafy plants; oral or injectable biotin supplement 

Human Health Risk — none 

Also Called — white comb 

Incidence — rare in North America 

System/Organ AFFECTED — comb 

Progression — spreads slowly 

Symi-toms - in growing and mature cocks with well-developed combs, usually of 
the Asiatic breeds: grayish white patches on comb that scale off (comb looks 
dusted with flour), thicken, and join to form a wrinkJed crust that smells 
moldy; sometim es crust spreads lo unleathered areas creating honeycomb 
appearance where feathers are lost, soon followed by depression, weakness, 
emaciation, and death 

Mortai.i rv — rare 

Postmortem Findings — spots, nodules, and yellowish cheesy deposits in diges- 
tive and upper respiratory tracts — miles, skin disorders due to poor nutrition 
Diagnosis — symptoms 
Cause — Microspomm gallinae fungus 

Transmission — contact with infecied birds or slougbed-off scales 

Prevention — improve nutrition and sanitation; breed for resistance 

Treatment — most birds recover in a few months without treatment; recovery 
may be hastened with daily liberal applications of anti- fungal or mange 
medication (for pets) until symptoms disappear 

Human Health Risk — scalp infection 
Flip-Over Disease. SeeSudden Death Syndrome 
Food Poisoning. See Botulism 
Fowl Cholera. See Cholera (acute), Cholera (chronic) 
Fowl Diphtheria. See Pox (wet) 
Fowl Pest. .See Influenza 
Fowl Plague. See Influenza 
Fowl Pox. So? Pox (dry) 
Fowl Spirochetosis. Sec Spirochetosis 
Fowl Typhoid. See Typhoid 

Also Called — trichothene mycotoxicosis 

Incidence — worldwide in temperate zones, but rare 

System/Organ Affected — digestive system and skin 

Incubation Period — accumulative 

Progression — acute 

Symptoms — in birds ol all ages: refusal to eat, slow growth, abnormal feathering, 

Gout (visceral) 273 

depression, bloody diarrhea, sores at corners of mouth and on skin, reduced 

resistance to respiratory diseases 

— in hens: sudden drastic drop in egg production, thin shells 
Percentage AFFECTED — high 
Mortality — low 

Postmortem Findings — sores in upper digestive tract, reddening throughout 

digestive tract, mottled liver, shriveled spleen 
Diagnosis — symptoms and feed analysis 

Cause — trichothecene (typeT-2) toxins produced by Fusarium xpomlricliioidex 

and other fungi in wheat, I've, millel, bai ley, corn, safflower seeds 
Transmission — poisoning due to eating contaminated feed; burning of skin 

coming into contact with caustic toxins 
Prevention — use commercially prepared pelleted feed 
Treatment — replace moldy feed 

i hat poison chickens 

Gangrenous Cellulitis/Dermatitis/Dermalomyositis. .See Necrotic Dermatitis 

Gapes. See"Gapeworm," page 88 

Gas Edema Disease. See Necrotic Dermatitis 

Gout (articular) 

Incidence — sporadic 

■System/Organ Affected — excretory system 
Incubation Period — long 
Progression — chronic 

Symptoms — in all ages: enlarged foot joints with pasty white urate deposits easily- 
seen through the skin 
Percentage AFFECTED — individual birds only 
Mortality — none 

Postmortem Findings — white tissue surrounding joints, white semi-fluid 

deposits within joints 
Resembles — no other disease 
Diagnosis — symptoms, postmortem findings 

Cause — abnormal accumulation of urates in the body due to kidney damage. 

excessive protein in diet, or hereditary susceptibility 
Transmission — genetic and/or related to nutrition 
Prevention — none known 
TREATMENT — none known 
Human Health Risk — none 
Gout (visceral) 

Also Called — acute gout, nephrosis, renal failure, renal gout, gout (visceral), 
visceral urate deposition 

System/Organ AFFECTED — kidneys 
Incubation Period — 14 days or more 

274 Gray Eye 

Progression — acute 

Symptoms — in chicks: flockwide deaths soon after hatch 

— in mature birds: sudden death ordeptession, weight loss, darkened head 
and shanks, white pasty diarrhea, cessation of laying, attempting to hide 
Percentage Affected — 1 to 5 percent 

Mortality — 2 to 4 percent per month, usually totaling no more than 50 percent 
but can be up to 100 percent 

Postmortem Findings — dry, shrunken breast muscles; both kidneys shriveled or 
one shriveled and one pale and swollen; chalky white needle-like crystals in 
kidneys and on surfaces of liver, abdominal fat, keel, and in joints 

Kesembles — any inflammation of the kidneys 

Diagnosis — symptoms, postmortem findings 

Guise — kidney failure due to inability to excrete urates for unknown reasons; 
possibly due to genetic defect, kidney damage from disease, water deprivation, 
fungal toxins, excessive dietary protein (30 to 40 percent), excess calcium (3 
percent or more), excess sodium-bicarbonate, calcium-phosphorus imbal- 
ance, vitamin A deficiency; sometimes follows bluecomb; often follows kidney 
damage due io infectious bronchitis 

Transmission — does not spread from bird to bird 

Prevention — provide plenty of pure drinking water, cool in summer and warm in 
protein rations 

Treatment— none if problem is genetic, otherwise improve nutrition 

Human Health Risk — none 
Gray Eye. SeeMarek's Disease 
The Greens. See Bluecomb 
Gumboro Disease. See Infectious Bursal Disease 


Heart Attack. See Sudden Death Syndrome 

Helicopter Syndrome. .See Infectious Stunting Syndrome 

Helminthiasis. See "Internal Parasites: Worms" (chapter 5) 

Hemophilus Infection. See Infectious Coryza 

Hemorrhagic Anemia Syndrome. See Infectious Anemia 

Hepatitis. See Blackhead. Campylobacteriosis. Infectious Anemia 

Histomoniasis. See Blackhead 


Incidence — worldwide but rare, in North America found only along Mississippi. 
Missouri, and Ohio rivers 

System/Organ Affected — entire body 

Incubation Period— 2 weeks 

Progression — acute or chronic 

Symptoms — all ages: emaciation, sometimes diarrhea 

Percentage Affected — low 

Mortality — 100 percent 

Postmortem Findings — mushy liver and spleen 

Infectious Anemia 275 

Diagnosis — laboratory identification of fungus 

Cause — Histoplasma capsitlatum fungus that proliferates in soil rich with the 

droppings of chickens and other birds 
Transmission — inhaled fungi 

Prevention — keep area free of dry accumulations of droppings from starlings 

and other birds 
Treatment — none 

Human Health Risk — possible respiratory infection from inhaled dust, see 
"Histoplasmosis," page 233 


IBD. See Infectious Bursal Disease 

Inclusion Body Hepatitis. See Infectious Anemia 

Infectious Anemia 

Also Called — adenoviral infection, aplastic anemia, chicken anemia agent 
infection, CAA infection, hemorrhagic anemia syndrome, HAS, hemorrhagic 
disease, hemorrhagic syndrome, inclusion body hepatitis, IBM 

Incidence — common in major chicken-producing countries, especially in 
commercial broiler flocks raised on reused litter 

System/Organ Affected — blood 

Incubation Period — 3 days 

Progression — acute, sudden onset with rapidly increasing deaths; lasts about 3 

Symptoms — in growing broilers. 3 to 20 weeks old (most often 5 to 9 weeks): 
sudden deaths of apparently healthy birds or depression, huddling, ruffled 
feathers, drawn -in head, pale comb, wattles, skin, and legs; sometimes 
diarrhea (may be bloody); death or recovery within 2 days 

Percentage Affected — usually low 

Mortality — 5 to 10 percent average, may be up to 40 percent during first 5 days 

Postmortem Findings — enlarged, pale, dull greenish, yellow, or tan liver mottled 
with red spots; bright red, watery blood; pale, yellow, fatly bone marrow; 
swollen, blood-filled kidneys tinged with yellow; pale muscles with pinpoint- 
sized bloody spots in muscles and organs; shriveled spleen and cloacal bursa — coccidiosis, infectious bursal disease, ulcerative enteritis, poisoning; 
aflatoxicosis, except that chickens are unlikely to be exposed to high enough 
doses of aflatoxin to produce these symptoms 

Diagnosis — flock history, symptoms (sudden deaths without symptoms), 
postmortem findings (fatty bone marrow, liver appearance), microscopic 
examination of liver 

Cause — unknown, possibly an adenovirus and/or a parvovirus called "chicken 
anemia agent;" may be related to vitamin K deficiency and/or drug toxicity 
(especially sulfa drugs); often found in combination with or following infec- 
tious bursal disease and/or secondary bacterial or fungal infections 

Transmission — ingesting bacteria from droppings of infected birds; spreads from 
breeders to chicks through hatching eggs; contaminated litter or equipment 
(especially hatching-egg cartons) 

276 Infectious Avian Encephalomyelitis 

Prevention — healthy birds in clean surroundings develop natural immunity after 
about 3 weeks of age; do not hatch eggs from breeders whose previous chicks 
had infectious anemia; vaccinate breeder flock for infectious bursal disease; 
avoid chilling, vaccinating, or prolonged use of sulfonamides in young birds; 
thoroughly clean contaminated facilities with disinfectant containing iodine 

Treatment — none other than supportive therapy (see page 192) including a 
supplement containing trace minerals and vitamins B and K; avoid coccid- 
iostats, which increase the disease's severity; treatment with antibiotics or 
sulfa drugs may worsen the disease 

Human Health Risk — none known 
Infectious Avian Encephalomyelitis. See Epidemic Tremor 
Infectious Bronchitis 

Also Called — avian infectious bronchitis, IB, mild cold 

Incidence — common worldwide 

System/Organ Affected — respiratory 

Incubation Period — 18 to 36 hours 

Progression — acute, starts suddenly, spreads rapidly, runs through flock in 24 to 

48 hours, individuals recover in 2 to 3 weeks 
Symptoms — in birds of all ages: gasping, coughing, sneezing, rattling, wet eyes, 

nasal discharge 

— in young and growing birds: watery nasal discharge, huddling near heat, 
loss of appetite, slow growth; sometimes swollen sinuses 

— in maturing birds: sometimes swollen wattles 

— in hens: sharp drop in laying to near zero, eggs with soft, thin, mis- 
shapen, rough, or ridged shells and watery whites 

Percentage Affected — 1 00 percent 

Mortality — limited in older birds; 25 percent in chicks, but can be up to 90 
percent, especially in cold weather and/or in the presence of a secondary 
bacterial infection 

Postmortem Findings — in chicks: yellowish cheesy plugs in throat; swollen, pale 

— in growing and mature birds: swollen, pale kidneys; urate crystals in 
tubes leading from kidneys; fluid yolk or whole eggs in abdominal cavity of 

Resembles — infectious laryngotracheitis, except that laryngo spreads less rapidly 
and is more severe; Newcastle, except dial Newcastle is more severe, produces 
a greater drop in egg production, and can cause nervous symptoms; infectious 
coryza, except that coryza often has a foul odor and produces facial swelling 
(bronchitis rarely does): egg drop syndrome, except that EDS does not cause 
runny egg whites; nutritional roup, except that roup does not affect egg whites 
or shells 

Diagnosis — difficult; symptoms, laboratory identification of virus 

Cause — several strains of coronavirus that survive no more than one week off 

chickens and are easily destroyed by disinfectants; infects only chickens, 

which vary in susceptibility among breeds and strains 
Transmission — the most contagious poultry disease; spreads by contact with 

Infectious Bursal Disease 277 

infected birds or their respiratory discharges; spreads on contaminated 
equipment; travels over 1 .000 yards through air 

Prevention — defies good management; avoid mixing birds of different ages or 
from different sources; vaccinate with strain(s) of virus found locally (infec- 
tious bronchitis may still occur due to a different or new strain of virus); be 
prepared to treat with broad-spectrum antibiotic if signs of air-sac disease 
follow vaccination; hens thai have a strong reaction to vaccine may never lay well 

Treatment — electrolytes in drinking water (see page 193); keep birds warm and 
well led; avoid crowding; watch for secondary bacterial infection, particularly 
air sac disease; survivors are permanently immune but become carriers (hens 
return to production in 6 to 8 weeks, but may never produce the same egg 
quality or quantity as before due to permanent ovary damage) 

Human Health Risk — none known, a different virus causes bronchitis in humans 
Infectious Bursal Disease 

Also Called — Gumboro disease, 1BD 

Incidence— common worldwide (except in New Zealand), primarily in large 

System/Organ Affected — lymph tissue, especially cloacal bursa 
Incubation Period — 1 to 3 days 

Progression — acute, appears suddenly, spreads rapidly, runs through flock in 1 
to 2 weeks 

Symptoms — in young birds 3 to 18 weeks old (most often broilers 3 to 6 weeks 
old): droopiness, ruffled feathers, vent picking (bird picks at own vent), 
straining while Irving to eliminate, whitish or watery (sometimes blood-tinged) 
diarrhea staining feathers below vent (making litter sticky), slight trembling, 
loss of appetite, dehydration, incoordination, fever followed by drop in body 
temperature to below normal, prostration, death 

Percentage Affected — nearly 100 percent 

Mortalit y — to 30 percent, peaking within a week; greater in Leghorns than in 
heavy breeds, in chicks fed 24 percent protein starter, and in birds infected 
with bronchitis, Newcastle, or cecal coccidiosis 

Postmortem Findings — none significant or dark, shriveled breasi muscles flecked 
with bloody streaks; mucus-tilled intestine; cloaca! bursa may be yellow, pink, 
red, or black, swollen, oblong-shaped, filled with creamy or cheesy material, 
and surrounded by gelatinous film (as die disease progresses, the bursa 
returns to normal size, then shrinks and shrivels up); swollen spleen covered 
with gray dots; birds that die from infection have swollen, pale kidneys 

Resembles — coccidiosis, except that cocci does not cause bloody flecks in 
muscles or swelling of cloacal bursa 

Dl\gnosis — flock history (age of birds, rapid onset, number of birds involved), 
symptoms (white or watery diarrhea, birds picking own vents, deadis peaking 
within a week, rapid recovery), postmortem findings (swollen or shriveled 
cloacal bursa) 

Cause — birnavirus thai affects primarily chickens and is common in every major 
poultry-producing area; survives in feed, water, and droppings for weeks and 
in housing for at least 4 months after removal of infected birds 

278 Infectious Catarrh 

Transmission — highly contagious; spread from infected birds through their 
droppings in contaminated litter and dusl in air. and on equipment, feed, 
shoes, insects, rodents, and wild birds; may be spread by darkling beetle, or 
lesser mealworm (Alphitobius diaperinus) found in litter 

Prevention — good sanitation helps but virus defies good management and is 
difficult to eradicate; vaccinated breeders pass temporary immunity to their 
chicks; natural immunity develops in chicks exposed to infection before the 
age of 2 weeks; vaccinate only where disease is prevalent 

Treatment — none; keep birds warm and well ventilated and provide plenty of 
drinking water; recovered chickens are more susceptible to other diseases and 
may not develop immune response to vaccines, especially Marek's 

Human Health Risk — none known 
Infectious Catarrh. See Infectious Coryza 
Infectious Coryza 

Also Called — cold, contagious catarrh, coryza, hemophilus infection, infectious 
catarrh, IC, roup 

Incidence — common worldwide, particularly in fall and winter in tropical and 

temperate climates (southeastern United States and California) 
System/Organ Affected — respiratory 
Incubation Period — 1 to 3 days 

Progression — acute and spreads rapidly or chronic and spreads slowly 
Symptoms — in chicks at least 4 weeks old: depression, nasal discharge, facial 

swelling, one or both eyes closed, death 

— in growing and mature birds (most likely group affected): watery eyes 

with eyelids stuck together, reddish foul-smelling discharge from nose, drop in 

feed and water consumption, drop in egg production, swollen face, eyes, and 

sinuses; sometimes diarrhea, rales or wheezing 
Percentage Affected — high (more in an acute outbreak than in a chronic 

Mortality — low 

Postmortem Findings — thick, grayish fluid, or yellowish solid material in nasal 

Face swollen with infectious coryza 

Infectious Laryngotracheitis 279 

Resembles — cholera, except that coryza causes facial swelling; chronic respiratory 
disease, infectious laryngolrncheitis, Newcastle, nutritional roup, infectious 
bronchitis, influenza, except that coryza produces a characteristic odor 

Diagnosis — symptoms (facial swelling, characteristic odor), laboratory identifica- 
tion of bacteria 

Cause — Haemophilus piimgallinaniin bacteria that do not survive long in the 
environment and are easily destroyed by disinfectants; often found in combi- 
nation with chronic respiratory disease, cholera, pox, infectious bronchitis, or 
infectious laryngotracheitis 

Transmission — contagious; contact with infected or carrier birds and their nasal 
or respiratory discharges in dust, drinking water, or feed 

Prevenhon — avoid combining birds from different flocks and of different age 
groups; remove infected birds, disinfect, and leave housing vacant for 3 weeks 
before bringing in new birds; vaccinate only if the disease has been positively 
identified; vaccinated breeders pass temporary immunity to their offspring; 
after an outbreak, clean and disinfect housing and leave vacant for a few days 

Treatment— erythromycin (Gallimycin), streptomycin (Vetstrep), sulfadimeth- 
oxine; disease may recur after treatment is discontinued; culling is preferable 
since survivors (including all birds in the flock) may be carriers 

Human Health Risk — none known 
Infectious Enterohepatitis. Sec Blackhead 
Infectious Hepatitis. SeeCampylobacteriosis 
Infectious Laryngotracheitis 

Also Called — avian diphlheria, ILT, laryngo, LT 

Incidence — common worldwide 

System/Organ Affected — upper respiratory tract 

Incubation Period — 6 to 12 days 

Progression — acute, spreads slowly, most birds die or recover Within 2 weeks, 
runs through flock in 2 to 6 weeks 

Symptoms— in maturing or mature birds (mild infection): watery inflamed eyes, 
swollen sinuses, nasal discharge, drop in egg production, unthriftiness 

— in maturing or mature birds (acute infection): nasal discharge, coughing 
(sometimes producing bloody mucus that gets on face or feathers), head 
shaking, breathing through mouth, gasping (neck extended during inhale, 
head on breast during exhale), choking, gurgling, rattling, whistling, or 
"cawing, " swollen sinuses and wattles, watery eyes, drop in egg production, 
soft-shelled eggs 

Percentage Affected— 5 percent in mild case, 90 to 100 percent in acute infection 
Mortality — 1 to 20 percent average, can be up to 70 percent in acute infection; 

least in young birds din ing warm weather, greatest in layers during winter 
Postmortem Findings — swollen windpipe clogged with bloody mucus or a cheesy 


Resembles — infectious bronchitis, except that laryngo spreads less rapidly and is 
more severe; Newcastle, except that laryngo does not cause nervous symp- 
toms; pox (wet), except that laryngo does not produce facial sores; swallowed 
feed-sack string wrapped around tongue, except thai string affects only one 

280 Infectious Leukemia 

bird at a time; gapeworm, except that in laryngo birds die more quickly with no 
worms in throat 

Diagnosis — flock history, symptoms (coughing up blood, high death rate), 

postmortem findings, confirmed by laboratory procedures 
Cause — a herpes virus that affects primarily chickens and pheasants and does 

not live long off the bird 
Transmission — highly contagious; inhaled virus from infected or catrier birds or 

contaminated litter; can be spread on equipment or the feet of rodents, dogs, 

and humans 

Prevention — (lock isolation and scrupulous sanitation; do not mix vaccinated or 
recovered birds with others; vaccinate //laryngo is common in your area, you 
show your chickens in areas where it is common, you regularly bring in new 
adult birds, or you frequently visit with chicken-keepers from laryngo- 
prevalent areas 

Treatment — none, cull; vaccination keeps disease from spreading and survivors 
are immune, but survivors (and vaccinated birds) are carriers; disinfect 
housing and leave it empty for 6 weeks; this is a reportable disease in many 
states, see "Reportable Diseases" page 196 
Human Health Risk — none known 
Infectious Leukemia. See Typhoid 
Infectious Sinusitis. See Chronic Respiratory Disease 
Infectious Stunting Syndrome 

Also Called — broiler runting syndrome, ISS, malabsorption syndrome, pale bird 

syndrome, split-wing syndrome, stunting syndrome, helicopter syndrome 
Incidence — increasingly more common in the United States, Europe, and Australia 
System/Organ Affected — digestive 
Incubation Period — 1 to 13 days 
Progression — chronic 

Symptoms — in 1 - to 6-week-old birds (primarily intensively raised broilers): 
uneven or seriously stunted growth (chicks reach only half their normal size by 
4 weeks of age) , pale skin, slow feather development; sometimes protruding 

and/or reluctance to walk (when disease occurs in combination with viral 

arthritis or osteoporosis) 
Percentage Affected — 5 to 20 percent 
Mortality — less than 6 percent, peaking early 

Postmortem Findings — enlarged, sometimes bloody stomach (proven triculus); 

pale, distended intestines; small intestine filled with poorly digested feed; 

sometimes thin, white, fibrous pancreas 
Resembles — infectious anemia, runting syndrome 
Diagnosis — symptoms, postmortem findings 

G\use — unknown, possibly due to a combination including one or more 
reoviruses and/or bacteria and/or fungal toxins; may occur in combination 
with encephalomalacia 

Transmission — unknown; possibly transmi tted by inhaling or ingesting virus gen- 
erated by infected birds; or spread from infected breeders through hatching eggs 

Infectious Synovitis 281 

PREVENTION — unknown; avoid crowd- 
ing and practice good sanitation 
Treatment — unknown; following an 

outbreak, thoroughly clean and 

disinfect housing with Iyeor0.5 

percent organic iodine solution 
Human Healti i Risk — none known 
Infectious Synovitis. See also 

Aiso Called — enlarged hock disease, 

Mycoplasma synoviae infection, MS 

(one form of mycoplasmosis) 
Incidence — worldwide but not , . 

. . .. Leg swollen with in eclions synovitis 

common except in large commercial 

flocks, especially in cold, damp weather 

System/Organ Affected — joints, sometimes upper respiratoiy tract 

Incubation Period — II to 21 days 

Progression — usually acute with slow recovery in young birds, chronic in older 
birds (survivors of acute form become chronic) 

Symptoms — in growing broilers, 4 to 12 weeks old: no signs or slow growth, 
lameness, pale comb, followed by depression, ruffled feathers, shrunken 
comb, hunkering around feeders and waterers, emaciation; sometimes 
swollen hocks, shanks, and foot pads (swollen areas feel hot), breast blister 
from squatting on floor, slight rales, bluish comb, green droppings capped 
with large amounts of white urate deposits 

Percent Affected — usually 100 percent, but only 15 to 20 percent have symptoms 

Mortality — up to 1 percent (usually due to secondary infection) 

POSTMORTEM FINDINGS — creamy yellowish or grayish fluid (acute) or thick orange 
yellow matter (chronic! in joints, keel, and fool pad; swollen, mottled, pale 
kidneys; enlarged, greenish liver — staphylococcic or viral arthritis, except that infectious synovitis 
more often involves wing joints and produces breast blisters 

Diagnosis — flock history, symptoms, postmortem findings, blood tests, labora- 
tory identification of bacteria 

Cause — Mycoplasma synoviae bacteria, often infecting following stress due to 
Newcastle or infectious bronchitis; may be caused by Escherichia coli, in which 
case some birds recover in about a week, others remain infected and become 

Transmission — inhaling bacteria from infected or carrier birds; spread by 

breeders through hatching eggs 
Prevention — keep litter dry; do not combine birds from different sources; 

acquire only MS-free stock; hatch eggs only from MS-free breeders; blood test 

and remove positive reactors; vaccinate where infection is prevalent (expensive) 
Treatment — none effective; aureomycin or terramycin in water or streptomycin 

by intramuscular injection may help, but survivors may be carriers 
Human Health Risk — none known 

282 Influenza 


Also Called — avian flu, avian influenza, AI, bird flu, European fowl pest, 
fowl plague 

Incidence — worldwide, but serious outbreaks are rare 
System/Organ Affected — primarily respiratory, sometimes involves diges- 
tive and nervous systems 
Incubation Period — a few hours to 3 days 

Progression — acute, spreads rapidly, runs through flock in 1 to 3 days 

Symptoms — in birds of all ages: sudden death without signs, or severe de- 
pression, droopiness, coughing, sneezing, rattling, watery eyes, huddling, 
ruffled feathers, loss of appetite, weight loss, reduced fertility, sudden 
drop in egg production, increased broodiness. eggs with soft or no shells, 
skin hemorrhages, fever; sometimes bloody nasal discharge, greenish 
diarrhea, darkened head, comb, wattles, and/or swollen eyes, comb, and 
wattles; sometimes twisted neck, loss of coordination, paralysis of legs or 
wings, swollen hock joints, purplish shanks; rapid deaths 

Percentage Affected — 100 percent 

Mortality — to 100 percent, usually low 

Postmortem Findings — none obvious; mild form: cheesy plugs in sinuses, 
throat, air sacs, oviduct 

— severe form: large and small reddish brown spots or blotches (hemor- 
rhages) along the interior of the upper and lower digestive tract, on the 
ovaries, and over the fat of the abdomen; straw-colored fluid beneath skin 
of face; enlarged blood vessels; loose gizzard lining 

Resembles — mild form: infectious bronchitis, chlamydiosis, chronic respira- 
tory disease, Newcastle 

— severe form: acute cholera, exotic. Newcastle, infectious laryngotracheitis 
Diagnosis — symptoms (high rate of rapid deaths), confirmed by laboratory 

identification of virus 

Cause — several strains of type A influenza orthomyxoviruses, some mild, 
some lethal, that affect a wide variety of bird species but do not survive 
long in the environment; often infect in combination with a bacterial or 
mycoplasmal disease 

Transmission — highly contagious; contact with infected birds (either do- 
mestic or wild) and their body discharges, especially droppings; spreads 
through improper disposal of infected birds and their manure, on con- 
taminated equipment and the feet of insects, rodents, and humans 

Prevention — during a local outbreak do not visit flocks or let people visit 
your flock; keep chickens indoors away from wild birds and water fre- 
quented by wild waterfowl; consult your vet about the availability of a 
vaccine against the virus responsible for the outbreak 

Treatment — mild form: antibiotic to prevent secondary bacterial or my- 
coplasmal infection; survivors are immune for several months but are 

— severe form: this is a reportable disease, see page 196 

Human Health Risk — the severe (highly pathogenic) form has the potential 
lor causing infection in humans and other mammals, but rarely does 

Leucocytozoonosis 283 


liltery Chicks. See Congenital Tremor 


Kinky Back 

Iritis. See Marek's Disease 

Keel Bursitis. See Breast Blister 
Keel Cyst. See Breast Blister 
Keratoconjunctivitis. See 

Also Called — spondylolisthesis 

Incidence — common in broiler 


Broiler with kinky back 

System/Organ Affected — joints or 

Symptoms — in broilers 3 to 6 weeks of age: arched back, extended neck, squatting 
with weight on hocks and tail, feet off the ground, struggling backward on 
hocks to move around (backpedaling), sometimes falling over with inability to 
get up, paralysis 

Percentage Affected — 2 percent 

Mortaijtv — 100 percent (due to dehydration) 

Postmortem Findings — deformed spinal column 

Resembles — any crippling condition including infection that causes swelling and 

pressure to the spinal cord 
Diagnosis — symptoms (few birds involved at once) 

Cause — unknown, possibly hereditary; rapid growth causes vertebrae to twist 

and pinch the spinal cord 
Transmission — genetic and/or feed related, does not spread from bird to bird 
Prevention — breed for resistance; do not feed for rapid growth 
Treatment — none, cull 
Human Health Risk — none 

Laryngotracheitis. See Infectious Laryngotracheitis 

Also Called — Leucocytozoon disease 

Incidence — only in areas where biting midges (Culicoides) and blackflies 
(Simuliidae) are prevalent, especially during summer and fall; in North 
America occurs in southeastern states, Minnesota, and Wisconsin 

System/Organ Affected — blood 

Progression — sudden onset, spreads rapidly, acute in young birds, chronic in 
mature birds 

Symptoms — in young birds (particularly those carrying heavy loads of internal 
parasites): droopiness, weakness, lameness, fever, loss of appetite, emaciation, 

- L - 

284 Leukosis/Sarcoma 

increased thirst, vomiting, increased excitability, rapid labored breathing, 
sometimes green diarrhea; birds recover or die within 3 days 

— in older birds: no symptoms but may remain carriers for months 
Percentage Affected — high 

Mortality — 10 to 80 percent 

Postmortem Findings — enlarged spleen, pale muscles and other tissues; some- 
times flabby, yellow flesh; often upper intestine filled widi blood 
Resembles — malaria 

Diagnosis — requires laboratory procedure (blood smear) 

birds more often than chickens 
Transmission — spread by biting midges from infected or carrier birds; does not 

spread through direct contact widi infected birds 
Prevention — control blackilies and midges (see page 62) or do not raise chickens 

in areas where they are abundant; isolate brooding chicks from infected adults; 

dispose of breeder Hock each year to eliminate carriers; continuous drug 

treatment (pyrimethamine in feed plus sulladimeihoxine or sulfaquinoxaline 

in feed or water) is a preventative but not a cure 
Treatment — ineffective; recovered birds are carriers, may be stunted, and will 

never lay well 
Human Health Risk — none known 
Leukosis/Sarcoma. See Lymphoid Leukosis, Osteopetrosis 
Limberneck. See Botulism 

Also Called — circling disease 

Incidence — worldwide in temperate areas, but rare (chickens are resistant) 
System/Organ Affected — brain and heart (encephalitic) or entire body 

Incubation Period — 5 to 15 days 
Progression — acute, moves through flock slowly 

Symptoms — in young birds: walking in circles with twisted neck (encephalitic 
form); diarrhea, gradual weight loss, death (septicemic form) 

— in mature birds: sudden deadi (septicemic) 
Percentage Affected — low 

Mortality — usually low but can reach 40 percent 
Postmortem Findings — patchy spots on liver; pale, inflamed heart 
Resembles — encephalitic form: encephalomalacia, epidemic tremor, exotic 

— septicemic form: any acute septicemia 
Diagnosis — difficult; laboratory identification of bacteria 

Cause — Listeria monocytogenes bacteria commonly found in soil and die bowels 

of birds and other animals 
Transmission — inhaling or ingesting bacteria; bacterial contamination of a 


Prevention — good sanitation 
Treatment— none, cull 

Lymphoid Leukosis 285 

Human Health Risk — conjunciivitis and listeric abortion from contact with 
infected or carrier birds; see "Listeriosis," page 236 
Liver Disease. SeeCampylobacteriosis 
Long-Bone Distortion. See Twisted Leg 
Lymphoid Leukosis 

Also Called — I' 

disease in the leukosis/ sarcoma group) 

Incidence — common worldwide 

System/Organ Affected — entire body 

Incubation Period — 14 weeks 

Progression — usually chronic 

Symptoms — in birds 16 weeks or older (especially those nearing maturity): 
depression, death 

— in birds over 6 months old: death without symptoms or pale shriveled 
comb, loss of appetite, diarrhea, emaciation, weakness; sometimes bluish 
comb, vent feathers spotted with white (urates) or green (bile); sometimes you 
can feel enlarged kidney, cloacal bursa, liver, or nodular tumors through skin 

Percentage Affected — sporadic 

Mortality — up to 25 percent (rapidly following first symptoms) 
Postmortem Findings — in birds 16 weeks or older: large and numerous soft, 
smooth, shiny white or gray tumors in liver, spleen, and cloacal bursa; some- 
times swollen grayish crumbly or gritty liver, enlarged joints, tumors in kidney, 
lungs, heart, bone marrow, testes or ovary 

Diagnosis — Hock history (birds' age), symptoms (progression and mortality), 
postmortem findings (especially involvement of cloacal bursa) 

Cause — a group of retroviruses that primarily infect chickens and do not live long 
off a bird's body 

Transmission — contact with infected birds; spreads from infected breeders 
through hatching eggs (main source of transmission) or by infected chicks to 
non-infected chicks through droppings; mechanically by blood-sucking 
parasites or unhygienic vaccination method 

Prevention — defies good management but can be controlled by; buying and 
breeding resistant strains (heavier meat breeds are more resistant that lighter 
laying breeds); identifying and eliminating breeders that produce infected 
chicks (requires testing for reactors); not reusing chick boxes; raising chicks on 
wire; not combining chickens of different ages or from different sources; 
thoroughly cleaning facilities before introducing new birds; Uioroughly 
cleaning and disinfecting incubator and brooder between hatches; controlling 
blood-sucking parasites; avoiding use of same needle for flockwide injections 
or vaccinations 

Treatment — none, cull; clean up and disinfect 

Human HEALTH Risk — none known 

286 Malabsorption Syndrome 


Malabsorption Syndrome. See Infectious Stunting Syndrome 

Also Called — avian plasmodia, Plasmodium infection 

Incidence — worldwide in temperate climates 

System/Organ Affected — blood 

Incubation Period — 5 to 7 days 

Progression — acute to chronic 

Symptoms — in all ages: none to death 

Percent 'age Affected — 5 to 20 percent 

Mortality — to 90 percent 

Postmortem Findings — anemia 

Resembles — leucocytozoonosis 

Diagnosis — laboratory testing (blood smear) 

Cause — Plasmodium spp protozoan parasites 

Transmission — mosquito biles 

Prevention — control mosquitoes; isolate chickens in mosquito-proof housing 

Treatment— none 

Human Health Risk — none known 
Marble Bone. Sec Osteopetrosis 
Marek's Disease 

Also Called — MD, neuritis, neurolymphomatosis. range paralysis (eye form: 
gray eye, iritis, ocular lymphomatosis, uveitis) 

Incidence — very common worldwide (more so in large breeds than in bantams) 

System/Organ Affected — organs (liver, lungs, and others), nerves, or skin; see 
page 1 27 for chart describing forms of Marek's disease 

Incubat ion Period — 2 weeks 

Progression — often acute 

Symptoms — in chicks over 3 weeks old (most commonly 12 to 30 weeks): growing 
thin while eating well (most common form), deaths starting at 8 to 10 weeks 
and persisting until 20 to 25 weeks 

— in maturing birds (6 to 9 months old): enlarged, reddened feather 
follicles or white bumps (tumors) on skin that scab over with a brown crust 
(skin form); stilted gait or lack of coordination, pale skin, wing or leg paralysis 
(involves nerve); when both legs are paralyzed, one points forward and the 
other points back under body; sometimes rapid weight loss, gaping or gasping, 
transient paralysis lasting 1 to 2 days (pseudo-botulism form), dehydration, 
emaciation, coma; death due to inability to get to food and water or trampling 
by other chickens 

— in breeds with reddish bay eyes: cloudy grayish, dilated, irregular pupil 
("gray eye," involves optic nerve); distorted or blinded eye 

— in all ages: sudden death of apparently healthy birds 
Percentage Affected — 30 to 50 percent in unvaccinated flocks, less than 5 

percent in vaccinated flocks 
Mortality — can be nearly 100 percent; gradually increasing for up to 1 weeks, 
higher in pullets than in cockerels 

Marek's Disease 287 

Chicken paralyzed with Marek's disease 

Postmortem Findings — in cases of sudden death, massive tumors, especially 
along the spinal column; otherwise, enlarged nerves with nodules (usually only 
on one side — compare same nerve on opposite side of body); tumors in testes 
or ovary (ovary takes on a "cauliflower" appearance); solidified lungs; ex- 
tremely enlarged liver, spleen, or kidneys with grayish while, soft areas; 
sometimes coarse, granular liver 

Resembles — primarily lymphoid leukosis (see page 128 for chart on how to tell 
the two apart); respiratory disease when Marek's affects the lungs; transient 
paralytic Marek's (called "pseudo-botulism" or "false botulism") resembles 
botulism, except that in pseudo-botulism birds recover quickly; paralysis and/ 
or internal changes may resemble blackhead, epidemic tremor, joint infection 
or injury, Newcastle disease, slipped tendon, riboflavin deficiency, tuberculo- 
sis, ortick paralysis (see "Soft Ticks," page 73) 

Diagnosis — flock history (birds not yet mature), symptoms (especially discolored 
iris and irregular pupil), postmortem findings (two or more Organs affected) 

Cause — six different herpes viruses concentrated in feather follicles, shed in 
dander, survive for years in dust and litter; In pullets, often infect in combina- 
tion with coccidiosis 

Transmission — contagious; contact with carrier or infected birds or their feathers; 
contact with contaminated litter; inhaled contaminated dust or dander; spread 
by darkling beetle or lesser mealworm (Alphitobius diaperinits) found in litter; 
not transmitted through hatching eggs or on their shells 

Prevention — breed for resistance (some chickens carry a resistance factor, "B21," 
detected through blood testing); practice good sanitation; provide good 
ventilation; brood chicks away from adult birds until 5 months of age (by 
which time they develop resistance); keep turkeys with chickens (turkeys carry 
a related though harmless virus that keeps Marek's virus from causing tumors); 
inject vaccine under skin lifted at nape of neck of newly hatched chicks, one- 
time vaccination confers lifetime immunity; do not expose vaccinated chicks 
to infection until immunity develops within 7 days; not all vaccines are 
effective against all six strains of Marek's virus 

Treatment — none, cull affected birds (unless you're breeding for resistance); 
some tumors, particularly those of the feather follicles, clear up and the bird 

288 Mesogenic Newcastle 

recovers on its own, but survivors are carriers 
Human Health Risk — none known from the virus, but handling vaccine may 

make your eyes itch for a few days 
Mesogenic Newcastle. See Newcastle Disease 
Moniliasis. See Thrush 
Monocytosis. See Bluecomb 
Mud Fever. See Bluecomb 
Muguet. See Thrush 

Muscular Dystrophy. See White Muscle Disease 

Mushy Chick Disease. See Omphalitis 

Mycoplasma gallisepticum. See Chronic Respiratory Disease 


Mycotoxicosis. SeeAflatoxicosis. Fusariotoxicosis, Ochratoxicosis 

- N - 

Navel Ill/Infection. See Omphalitis 

Necrotic Dermatitis 

Also Called — avian malignant edema, clostridial dermatomyositis, gangrenous 
cellulitis, gangrenous dermatitis, gangrenous dermatomyositis, gas edema 
disease, wing rot 

Incidence — worldwide but rare 

System/Organ Affected — skin 

Incubation Period — 2 to 3 days 

Progression — acute 

Symptoms — in birds 3 to 20 weeks old (commonly 4 to 8 weeks old): sudden 
deaths (sometimes with small, moist sores between toes) or depression, 
lameness, incoordination, prostration, loose feathers or skin that easily rubs 
off; skin that pops or crackles when rubbed (due to gas underneath); reddish 
black patches of dead, featherless skin on wings, breast, abdomen, or legs; 
death within 24 hours, body decomposes rapidly, turning green within 1 or 2 

Percentage Affected — low 
Mortality — 60 to 100 percent 

Postmortem Findings — bloody, gelatinous fluid beneath skin; gray or tan breast 
and thigh muscles that look cooked; usually shriveled cloacal bursa; some- 
limes enlarged liver and spleen, swollen kidneys, degenerated lungs 

Resembles — blister burn or contact dermatitis caused by wet or improperly 
managed litter; nutritional deficiencies leaving skin unprotected due to slow 

Diagnosis — symptoms, postmortem findings 
Cause — Clostridium septicum bacteria commonly foi 

litter, feed; often occurs in combination with necrotic enteritis, 

Nephrosis 289 

staphylococcosis, and colibacillosis; usually follows an outbreak of infectious 
bursal disease, sometimes follows infectious anemia or infectious stunting 

Transmission — through wounds caused by caponizing, fighting, cannibalism, 

injury on poorly designed equipment 
PREVENTION — good sanital ion and nutrition; good management to avoid wounds; 

ventilation to prevent excessive humidity in housing; breed for resistance to 

infectious bursal disease 
Treatment— broad -spectrum antibiotic (penicillin, erythromycin, tetracyclines), 

proper selection requires laboratory identification of all organisms involved; 

vitamin-electrolyte supplement hastens recovery 

Necrotic Enteritis 

Also Called — cauliflower gut, crud.enterotoxemia, NE, rot gut 
Incidence — worldwide but rare 
System/Organ affected — intestines 
Incubation Period— 3 to 10 days 

Progression — acute, appears suddenly, progresses rapidly, runs through flock in 
5 to 10 days 

Symptoms — in intensively raised birds, 2 weeks to fi months old (commonly 2 to 5 
weeks old): depression, loss of appetite, ruffled feathers, reluctance to move, 
diarrhea, death within hours; or sudden death without symptoms 

Percentage Affected— up to 15 percent 

Mortality — 2 to 50 percent 

Postmortem Findings — cauliflower-like yellow or green membrane lining small 

intestine filled with gas or foul-smelling brown fluid 
Resembles — intestinal coccidiosis (Eimeiiti bniiuHti), except that cocci is usually 

less severe; ulcerative enteritis, except that necrotic enteritis rarely affects the 

cecum or liver 

Diagnosis — postmortem findings, laboratory identification of bacteria 

Cause — Clostridium peifringens bacteria and their toxins, sometimes following 

change in feed; often found in conjunction with coccidiosis and occasionally 

salmonellosis (both of which increase susceptibility) 
Transmission — droppings from infecied birds and spores in built-up litter, dust, 

or feed 

PREVENTION — good sanitation management to prevent coccidiosis and other 

intestinal infections; make feed changes gradually 
TREATMENT — bacitracin in drinking water at the rate of l A gram per gallon for 4 

days, combined with amprolium to control coccidia; vitamin supplement 

following treatment hastens recovery 
Human Health Risk — do not slaughter sick birds: toxins in meat contaminated by 

infected droppings during butchering can cause mild to serious illness; see 

"Clostridium Poisoning," page 241 
Nephrosis. See Gout (visceral), Infectious Bursal Disease 

290 Neuritis 

Neuritis. See Marek's Disease 
Neurolymphomatosis. See Marek's Disease 

Neurotropic Velogenic Newcastle Disease. See Newcastle Disease (exotic) 
Newcastle Disease 

Also Called — avian distemper, domestic Newcastle, endemic Newcastle. 

parainfluenza, pneumoenceplialitis. pseudofowi pest, mesogenic Newcastle, 

mild Newcastle, ND 
Incidence — common worldwide 

System/Organ Affected — respiratory and nervous systems 
Incubation Period — 2 to 15 days (5 to 6 average) 

Progression — acute, starts suddenly, spreads rapidly, runs through flock in 
about a week 

Symptoms — in growing birds: wheezing, gasping, coughing, chirping, sometimes 
followed within 10 to 14 days by nervous disorders (drooping wing, draggy leg, 
twisted neck), death due to being trampled by other chickens 

— in mature birds: slight wheezing, temporary cessation of laying, eggs with 
soft, rough, or deformed shells: sometimes nasal discharge, cloudy eye 

Percentage Affected — high 

Mortality — few or none but can be high when nervous symptoms appear 

POSTMORTEM Findings — none significant; sometimes mucus in throat and 
thickened air sacs containing yellowish matter 

Resembles — infectious bronchitis and other respiratory diseases, except that 
Newcastle produces nervous symptoms; a disease known as "fowl plague" that 
does not occur in North America 

Diagnosis — symptoms (chicks with both nervous and respiratory signs), labora- 
tory identification of virus 

Cause — paramyxovirus that affects many different birds 

Transmission — contagious; spread by inhaling or ingesting the virus from body 
excretions of infected birds or carriers in air, water, or feed 

Prevention — defies good management; breed for genetic resistance (tests for 
antibodies against the virus commonly find healthy reactors, suggesting a high 
degree of resistance); vaccination not necessary unless virus is common in 
your area, then vaccinate chicks at 1 day old (or between 7 and 10 days) and 
repeat every 4 months or as required by risk of exposure; vaccinate all adult 
birds when chicks are first vaccinated 

Treatmen t — keep birds warm and well fed; watch for secondary bacterial 
infections, particularly air-sac disease and chronic respiratory disease; 
survivors are immune but will be carriers for up to a month 

Human Health Risk — lemporary (3 to 7 days) eye infection may result from 
handling vaccine or infected birds 
Newcastle Disease (exotic) 

Also Called — Asiatic Newcastle disease, neurotropic velogenic Newcastle 
disease, NVND, the plague (in the Philippines), pseudo-poultry plague, 

Incidence — rare but worldwide, especially in young, concentrated, confined flocks 

Newcastle Disease (exotic) 29 1 

System / Organ Affected — respiratory and nervous systems, sometimes digestive 

Progression — acute, spreads rapidly, runs through Bock in 3 to 4 days, lasts 3 to 4 

Symptoms — in all ages: sudden, high rate of death widtout symptoms or 

— in chicks: gasping, sneezing, coughing, "chirping" sound, rattle in throat; 
followed by slow growth, drooping wings, dragging legs; sometimes twisted 
head and neck, circling, somersaulting, walking backward, paralysis; birds 
recovering from respiratory symptoms but retaining nervous symptoms 

— in mature birds: listlessness, rapid or difficult breathing, progressive 
weakness, near total cessation of laying within 3 days (sometimes shells have 
odd shapes or colors with flabby, blood-stained yolks and watery whites); 
followed by loss of coordination, loss of appetite, muscular tremors, twisted 
neck, wing and leg paralysis; sometimes watery, greenish (blood-stained) 
diarrhea, swollen, blackish eyes with straw-colored fluid draining from eyes 
and nose, bleeding through nose, death within 2 to 3 days 

Percentage AFFECTED — up to 100 percent 

Mortality — usually 50 percent in adults. 90 percent in young birds, can be 100 
percent in all ages 

Postmortem Findings — yellow patches on roof of mouth; large and small reddish 
brown spots or blotches (hemorrhages) in the upper and lower digestive tract, 
over abdominal fat, and on the ovary; wrinkled or discolored yolks; broken egg 
in abdominal cavity of hens 

Resembles — aflatoxicosis, blackhead, canker, coccidiosis, acute cholera, influ- 
enza, infectious laryngotracheitis, mild Newcastle, nutritional roup, thrush 

Diagnosis — flock history (human handler's contact with infected chickens or 
smuggled cage bird), symptoms, postmortem findings, confirmed by labora- 
tory identification of virus 

Cause — several strains of paramyxovirus that survive for up to 30 days in broken 
eggs, feathers, drinking water, and droppings in litter, but are sensitive to 

Transmission — highly contagious; usually introduced by illegally imported cage 
birds that have not gone through USDA quarantine; spread by contact with 
infected birds and their body discharges; spreads in feed, water, air, and on 
equipment and the feel of rodents and humans; eggs laid by infected hens 
rarely hatch but may break in incubator and spread the virus 

Prevention — avoid mixing birds of different ages or from different sources; avoid 
contact with illegally imported birds; do not visit flocks or let people visit your 
flock if an outbreak occurs in your area; vaccination does not offer 100 percent 

Treatment — none; this is a reportable disease, see "Reportable Diseases" page 
196; infected flocks are quarantined and destroyed; dtoroughly clean up and 


compound, or 5 to 20 percent chlorine bleach 


292 New England Disease 

Human Health Risk — temporary (3 to 7 days) eye infection requiring medical 
treatment may result from handling vaccine or infected birds 
New England Disease. See Epidemic Tremor 
New Wheat Disease. See Bluecomb 
Nutritional Myopathy. See White Muscle Disease 

-O - 


Incidence — sporadic in North America, Europe, and Asia 
System/Organ Affected — kidney 
Progression — gradual and cumulative 
Symptoms — in hens: yellow diarrhea, thin-shelled eggs 
Percentage Affected — 5 to 50 percent, depending on age of birds and level of 

Mortality — usually low, depending on amount of toxin ingested 

Postmortem Findings — swollen, pale kidneys, sometimes swollen, spotted liver, 

intestine filled with mucus 
Resembles — other mycotoxicoses 

Diagnosis — symptoms, postmortem findings, feed analysis 

Cause — ochratoxins produced by Aspergillus ochraceous and Penicillium 

viridiccttum fungi in barley, corn, sorghum, and wheat and in pelleted feed 

made with contaminated grain 
Transmission — poisoning from contaminated rations; does not spread from bird 

to bird 

Prevention — avoid moldy feeds 
Treatment — replace contaminated feed 

Human Health Risk — danger of ochratoxin residue in meat is low as most of the 
toxin is rapidly excreted in droppings; residue rarely appears in eggs 
Ocular Lymphomatosis. SezMarek's Disease 
Oidica. See Thrush 
Oidiomycosis. See Thrush 

Also Called — mushy chick disease, navel ill. navel infection (one form of 

Incidence — common 
System/Organ Affected — navel 

Incubation Period — 1 to 2 days (present at time of hatch) 
Progression — acute 

Symptoms — dead embryos late in incubation; newly hatched chicks feel wet 
— in chicks to 4 weeks of age: drooping head, puffed-up down, huddling 
near heat, lack of uniformity in size, lack of interest in food or water, distended 
abdomen with unabsorbed yolk sac; unhealed, reddened, swollen, and wet, 
mushy or scabby navel; sometimes diarrhea; death 

Percentage Affected — usually low unless incubator sanitation is poor 


Chick infected with 

Mortality — up to 15 percent, starting just prior to 

hatch and continuing for up to 3 weeks; may 

increase as hatching season progresses 
Postmortem Findings — incompletely healed navel, 

fluid under skin, bluish abdomen, unabsorhed yolk 

in abdomen (sometimes yellowish green and watery 

or yellowish brown and cheese-like, often bad 


Diagnosis — symptoms, postmortem findings 
Cause — Esclierichia coli combined with Staphylococcus 

aureus. Streptococcus faecalis, and odier bacteria 
Transmission — contaminated droppings on hatching 

eggs; high incubation humidity keeps navel from 

closing properly, infectious organisms in incubator 

or brooder (or within egg, having penetrated shell 

before or during incubation) enter unhealed navel; 

feed, water, litter contaminated with droppings; not 

transmitted between growing or mature birds 
Prevention — hatch only clean, uncracked eggs; control 

incubator humidity; clean and disinfect incubator 

and brooder between hatches 
Treatment — none effective, cull; if newly purchased chicks experience a high 

death rate, notify seller and/or hatchery 
Human Health Risk — none, if good sanitation is practiced after handling infectec 


Ornithosis. See Chlamydiosis 
Osteomalacia. See Rickets 

Also Called — marble bone, thick leg disease (one disease in the lymphoid/ 

sarcoma group) 
Incidence — common 
System /Organ Affected — bones 
Incubation Period — 30 days 
Progression — usually chronic 

Symptoms — in young or mature birds (more often male than female): thickened 
(sometimes unusually warm) leg bones, puffy looking shanks, lameness or 
stilted gait, faulty body conformation, stunting 

Percentage Affected — low 

Mortality' — up to 10 percent 

Postmortem Findings — thickened, deformed bones — rickets, except that osteopetrosis does not cause bones to become 
porous; ca 

Cause — 

294 Osteoporosis 

Transmission — contact with infected birds; spread by infected breeders through 
hatching eggs or by infected chicks to non-infected chicks through droppings; 
mechanically by bloodsucking parasites or unhygienic vaccination method 

Prevention — defies good management but can be controlled by: buying and 
breeding resistant strains; identifying and eliminating breeders that produce 
infected chicks (requires testing for reactors); not reusing chick boxes; raising 
chicks on wire; not combining chickens of different ages or from different 
sources; thoroughly cleaning facilities before introducing new birds; thor- 
oughly cleaning and disinfecting incubator and brooder between hatches; 
controlling bloodsucking parasites; avoiding flockvvide injections or vaccina- 
tions using one needle 

Treatment — none, cull; clean up and disinfect 

Human Health Risk — none known 
Osteoporosis. See Cage Fatigue 


Pale Bird Syndrome. See Infectious Slunting Syndrome 
Paracolon. See Arizonosis 
Parainfluenza. 5eeNewcastie Disease 

Also Called — paratyphoid infection, PT (one kind of salmonellosis) 
Incidence — very common worldwide 

System/Organ Affected — digestive or entire body (septicemic) 
Incubation Period — 5 days 
Progression — acute or chronic 

Symptoms — in embryos al time of hatch: numerous dead in shell, pipped or 

— in chicks up to 5 weeks old: death at time of hatch or depression, 
weakness, poor growth, drooping wings, decreased appetite, increased thirst, 
"chirping" or "peeping" sounds, huddling around heat with feathers ruffled, 
eyes closed, head down, wings drooping; sometimes swollen joints, swelling or 
blindness in one or both eyes, watery diarrhea with pasting, dehydration 

— in adult carriers: no symptoms or reduced egg production; purplish 
head, comb, and wattles (septicemic form) 

Percentage Affected — high 

Mortality — 10 to 20 percent, sometimes 100 percent; peaks at 6 to 10 days of age 
Postmortem Findings — in chicks: none recognizable, or unabsorbed yolk sac, 

dehydration, swollen liver with red streaks or white dots, creamy or yellowish 

cheesy cores in ceca 

— in adult birds: none recognizable, or inflamed intestine, swollen liver, 
spleen, kidneys 

Resembles — arizonosis, typhoid, pullorum, seplicemia due to colibacillosis (see 
"Colibacillosis," page 112), infectious synovitis when joints are swollen 

Diagnosis — flock history (birds' age), symptoms, postmortem findings, labora- 
tory identification of bacteria 

Pediculosis 295 

Cause — over 150 different Salmonella bacteria (S. heidelberg and S. typhi murium 
most commonly affect chickens. S. enlei iiidis also affects humans) that reside 
in soil and litter and infect a variety of birds and mammals 

Transmission — contaminated soil or litter (persists for up to 7 months); contami- 
nated droppings (persists for up lo 28 months); contaminated feathers, dust, 
hatchery fluff (persists for up to 5 years); feed containing contaminated animal 
by-products (not including pellets and crumbles) or feed and water containing 
contaminated droppings; spreads from infected breeders to chicks through 
hatching eggs (eggs can blow up during incubation, further spreading con- 
lamination); spread on dirty equipment, feet of rodents and humans 

Prevention — difficult, due to bacteria's wide range of animal hosts; collect 
hatching eggs often; hatch only eggs from paratyphoid-free breeders: replace 
nesting litter often; clean and disinfect incubator and brooder after each hatch; 
minimize chilling, overheating, parasitism, withholding of water or feed; keep 
drinking water free of droppings; control rodents, reptiles, wild birds, cock- 
roaches, beetles, fleas, and flies; avoid mixing chickens of various age groups; 
keep breeders on wire flooring 

Treatment — none effective, survivors may be carriers; Salmonella Iznteriiidis 
infection is reportable, see "Reportable Diseases" page 196 

Human Health Risk — mild to serious illness from eating raw or undercooked 
contaminated meat or eggs, see "Salmonellosis," page 239 
Parrot Fever. See Chlamydiosis 
Pasted Vent 

Also Called — cloacitis, vent gleet 

Incidence — common in chicks, less common in mature birds 
System/Organ Affected — vent 
Progression — chronic 

Symptoms — in chicks up to 10 days old: droopiness, droppings sticking to vent 
— in laying hens: offensive odor from droppings sticking to vent feathers 
Percentage Affected — usually limited 
Mortality — possible, if vent gets sealed shut 
Postmortem Findings — distended rectum filled with droppings 
Resembles — in chicks: arizonosis and paratyphoid, except that pasted vent 

involves fewer chicks and they appear otherwise healthy 
Diagnosis — symptoms 

Cause — in chicks: unknown, may be due to improper consistency of droppings 
caused by rations or chilling 

— in hens: loss of muscle tone due to hereditary weakness 
Transmission — does not spread from bird to bird 

Prevention — keep chicks warm; do not hatch eggs from affected hens to avoid 
passing on hereditary weakness 

Treatment — can 

Human Health Risk — none 
Pasteurellosis. See Cholera (acute); Cholera (chronic) 
Pediculosis. See-Lice," page 63 

296 Pendulous Crop 

Plantar Pododermatitis. See Bumbiefoot 
Plasmodium Infection. See Malaria 

Pleuropneumonialike Organism (PPLO) Infection. See Chronic Respiratory Disease 
Pneumoencephalitis. See Newcastle Disease 


Incidence — common in some areas worldwide, especially in confined flocks in 

cold weather 
System/Organ Aefected — skin 
Incubation Period— 4 to 14 days 

Progression — spreads slowly (except when spread by mosquitoes), lasts 3 to 5 
weeks in individual birds 

Symptoms — in birds of all ages, except newly hatched chicks: raised clear or 
whitish wart-like bumps on comb and wattles that grow larger, turn yellowish, 
and later become reddish brown, gray, or black bleeding scabs appearing 
singly, in clusters, or clumping together; scabs fall off to form smooth scars; 
sometimes scabs spread to eyelids, unfeathered areas of head and neck, vent 
area, feet, or legs; retarded growth or weight loss (sores around eyes inhibit 
feeding), drop in egg production 

Percentage Affected — low to 100 percent 

Mortality — 1 to 2 percent — comb wounds due to fighting, except that wounds do not spread 
Diagnosis — symptoms, confirmed by laboratory identification of virus 
Cause — pox virus that affects a wide variety of birds and survives for many 

months on scabs and feathers of infected birds 
Transmission — through skin wounds (due to insect biles, dubbing, lighting, 
cannibalism, or other injury); spreads by means of feathers and scabs from 
infected birds; spread mechanically by mites, mosquitoes, and wild birds; may 
spread from infected breeders to chicks through hatching eggs, causing 
disease when infected birds come under stress 
Prevention — defies good management; control mites and mosquitoes; vaccinate 
where pox is prevalent (on day-old chicks, use only vaccine designated for 
chicks); if large number of vaccination sites do not swell and scab over within 7 
to 10 days, revaccinate with new batch of vaccine; since pox spreads slowly, it 
may be checked by vaccinating while disease is in progress 

around mouih and eyes so birds can eat; prevent secondary infection with 300 

Poisoning. Seepage 139 
Pox (dry) 

Also Called — avian pox, chii 
pox), cutaneous pox, fowl 

Pox (wet) 297 

mg oxytetracycline (Terramycin) per gallon of drinking water for 3 days 
followed by vitamin supplement in water; infected birds naturally recover in 2 
to 4 weeks and are immune (but some remain carriers and may become 
reinfected during molt and other times of stress); thoroughly clean housing 
after outbreak to remove all infective scabs 
Human Health Risk — none known; "chicken pox" in humans is caused by a 
different virus that has nothing to do with chickens 
Pox (wet) 

Also Called — diphtheritic pox, fowl diphtheria 
Incidence — worldwide, less common than dry pox 
System/Organ Affected — upper respiratory 
Incubation Period — 4 to 14 days 

Progression — spreads slowly (except when spread by mosquitoes) , lasts 3 to 5 
weeks in individual birds 

Symptoms — in birds of all ages, except newly hatched chicks: transparent whitish 
wart-like orscabby bumps on face, eyes (can cause blindness), throat, and 
windpipe (possibly becoming large enough to suffocate bird), growing larger 
until they join and turn yellow and cheesy; raies or wheezing, nasal or eye 
discharge, death due to suffocation 

Percentage Affected — low to 100 percent 

Mortality — up to 50 percent 

Postmortem Findings — yellowish or brownish cheesy masses in mouth, upper 

throat, and windpipe, anchored by cheese-like roots 
Resembles — infectious laryngo tracheitis, nutritional roup 

— in chicks: biolin deficiency, canker 
Diagnosis — flock history, symptoms, confirmed by postmortem findings, 

laboratory identification of virus 
Cause — same vims as dry pox invading the upper respiratory tract 
Transmission — same as for dry pox 
Prevention — same as for dry pox 

Treatment — if thick discharge interferes with breathing, clear airways with 

Head of a chicken 
with pox 

298 Pseudo-Botulism 

cotton swab coated with iodine; otherwise, treat as for dry pox 
Human Health Risk— none known, not related to diphtheria in humans 

Pseudo-Botulism. SeeMareks Disease 

Prolapse. See "Prolapsed Oviduct," page 53 

Pseudofowl Pest. See Newcastle Disease 

Incidence — rare 

System/Okgan Affected — entire body 

Incubation Period — 3 days 

PROGRESSION — acute to chronic 

Symptoms — in embryos or newly hatched chicks: death 

— in older hirds: lameness, loss of coordination, swollen head and wattles, 
swollen hock joints and foot pads, diarrhea, death within 1 to 2 days 
Percentage Affected — up to 10 percent 

Mortality — usually no more than 10 percent but can be up to 90 percent 
POSTMORTEM Findings — swollen, spotty liver, spleen, kidneys 
Resembles — septicemic eolibacillosis 

Diagnosis — characteristic fruity odor, laboratory identification of bacteria 
CAUSE — Pseudomonas aeruginosa bacteria commonly found in chicken drop- 
pings, soil, water, and humid environments; infects birds with reduced 
resistance due to some other cause 
Transmission — droppings of infected birds in feed, water, litter; infects chicks 
through shells of hatching eggs; spreads in vaccines and antibiotics handled in 
an unhygienic manner; infects chickens with reduced susceptibility due to 
other bacterial or viral diseases 
Prevention — good incubator and brooder sanitation; hygienic handling of 
vaccines and antibiotics; avoid mixing birds of different ages; avoid stress 
Treatment — bacteria are resistant to many antibiotics, but treatment may reduce 
losses //started early and a suitable antibiotic (sudi as gentamicin) is deter- 
mined through laboratory sensitivity testing 
Human Health Risk — rare but potentially serious infection due to bacteria 
entering an open wound or deep puncture 
Pseudo-Poultry Plague. See Newcastle Disease 
Psittacosis. SeeChlamydiosis 
Pullet Disease. See Muecomb 

Also Called — bacillary white diarrhea, BWD, pullorum disease, PD, white 

diarrhea (one kind of salmonellosis) 
Incidence — worldwide, rare in North America 
System/Organ Affected — digestive or septicemic 
Incubation Period— 7 to 10 days 
Progression — acute or chronic 

Symptoms — in chicks up to 4 weeks old: sudden death or loss of appelite, 
sleepiness, weakness, huddling near heat, swollen hock joints, white (or 
greenish-brown) pasty diarrhea; sometimes gasping, shrill peeping or chirping 
while trying to expel droppings: uneven growth among survivors 

Reovirus Infection 299 

— in mature birds: no signs or loss of appetite, increased thirst; sometimes 
pale, shriveled comb, green diarrhea, drop in egg production 

Percentage Affected — up to 100 percent 

Mortality — up to 90 percent in chicks, increasing on 4th or 5th day and peaking 

at 2 to 3 weeks of age (1 00 percent if infected chicks are shipped, chilled, or 

kept in unsanitary conditions) 
Postmortem Findings — in chicks: none recognizable; or unabsorbed yolk; cheesy 

material in abdominal cavity or ceca; enlarged liver, heart, kidneys, and spleen; 

small white or gray nodules (pinpoint to pea-size) in liver, heart, gizzard, 

intestine, and lungs 

— in adult birds: none recognizable; or enlarged liver, heart, spleen, and 
kidneys; swollen ceca or oviduct filled with firm, cheesy material 

— in hens: brownish or greenish shriveled yolks, yolk material in abdominal 

— in cocks: shriveled testes (testicles) 

Resembles — omphalitis, paratyphoid, typhoid; white diarrhea due to simple 

Diagnosis — history (birds' age), symptoms (pattern of deaths), laboratory 
identification of bacteria 

Cause — Salmonella ptiUorum bacteria, survives lor years in dry litter, but is easily 
destroyed by cleaning and disinfection 

Transmission — from infected breeders to chicks through hatching eggs; spread 
from chick to chick in incubator or brooder; occasionally transmitted by 
contaminated litter, shoes, equipment 

Prevention — purchase certified pullorum-free stock; hatch eggs only from 
pullorum-free breeders; do not mix certified pullorum-free stock with other 
birds; control flies, rodents, and wild birds; breed for resistance (heavy breeds 
such as Rocks and Reds are more susceptible than Leghorns and other light 
breeds); blood test birds (home kits are available) and eliminate carriers until 
two tests, no less than 21 days apart, are negative (some states require blood 
testing of all exhibition birds) 

Treatment— cull, survivors are carriers; this is a reportable disease in most 
states, see "Reportable Diseases ' page 196 

Human Health Risk — eating highly contaminated meat can cause acute intesti- 
nal infection (characterized by explosive onset, high fever, and prostration); 
recovery is spontaneous and rapid 
Pulmonary Aspergillosis. See Aspergillosis (acute). Aspergillosis (chronic)] 


Quail Disease. See Ulcerative Enteritis 

- R - 

Rachitic Chicks. See Rickets 
Range Paralysis. SeeMarek's Disease 
Renal Failure/Gout. See Gout (visceral) 
Reovirus Infection. See Viral Arthritis 

300 Reticuloendotheliosis 

Reticuloendotheliosis. Sec Hunting Syndrome 


Also Called — osteomalacia, rachitic chicks 

Incidence — rare, yet the most common nutritional deficiency of growing birds, 

especially those housed in confinement 
System/Organ Affected — bones 
Progression — depends on degree of deficiency 

SYMPTOMS — in young birds: depression, frequent squatting, stiff-legged gait or 
inability to stand, slow growth, ruffled feathers, black feather parts in red or 
buff breeds, easily benclable beak, bowed or twisted legs and wings, enlarged 
joints, paralysis 

— in mature birds: easily broken bones, bent keel dished in near the middle 
Percentage Affected — can be high 
Mortality — up to 20 percent 

Postmortem Findings — soft, rubbery bones, string of round knobs caused by 
beading of inner surfaces of rib heads where ribs join spine {called "rickety 
rosary" or "rachitic rosary") 

Resembles — cage fatigue, except that birds need not be in cages to get rickets 

Diagnosis — flock history (birds' age), symptoms (especially soft beak), postmor- 
tem findings (especially rib beading), ration evaluation 

Cause — deficiency of vitamin D3; deficiency or imbalance of calcium or phos- 
phorus (too much calcium ties up phosphorus); inability to absorb nutrients 
due to infectious stunting syndrome 

Transmission — nuiritional, does not spread from bird to bird 

Prevention — feed oyster shell or coarse limestone free choice; use commercially 
prepared ration fortified with vitamin Do; let birds out into the sunshine; range 
birds on legume or legume-grass pasture 

Treatment — vitamin D3 supplement at three times the normal amount for3 
weeks, then reduce to normal amount (take care, excess vitamin D in feed can 

Bent beak from rickets 

Round Heart Disease 30 1 

Bended ribs from rickets 

be toxic); for chicks, one-time dose of 1 5,000 IU vitamin D3; in case of paraly- 
sis, give a calcium phosphate supplement 
Human HEALTH Risk — none 
Rotaviral Enteritis 

Also Called — rotaviral infection, viral enteritis 
Incidence — worldwide and increasingly more common 
System/Organ Affected — digestive 
Incubation Period — 2 to 5 days 
Progression — lasts 5 to 10 days 

Symptoms — in young birds: depression, profuse watery diarrhea, inflamed vent, 

appetite loss, weight loss, dehydration, death 
Percentage Affected — nearly 1 00 percent 
Mortality — up to 50 percent 

Postmortem Findings — yellowish, watery, gas-filled matter in intestines and ceca 
Resembles — any other (enteric) disease causing diarrhea 
Diagnosis — laboratory identification of diarrhea's cause 

Cause — rotavirus common in the poultry environment, but doesn't always cause 

Transmission — contact with infected birds and their droppings; spreads on 
contaminated equipment; maybe transmitted in or on hatching eggs 

Prevention — clean and disinfect housing periodically; do not start new chickens 
on used litter 

Treatment — none, cull; penicillin and supportive therapy (see page 192) help, 
but survivors do not grow well; thoroughly clean and disinfect before introduc- 
ing new flock 
Human Health Risk — none known 
Rot Gut. See Necrotic Enteritis 
Round Heart Disease 

Incidence — extremely rare and only during winter in birds maintained on deep 

System/Organ Affected — heart 

302 Roup 

sion — acute 

Symptoms — in birds 4 to 8 months old: sudden death 
Percentage Affected — no illness evident 
Mort ality — up to 50 percent 
Postmortem Findings — enlarged, yellowish, soft heart, rounded at the tip 

sions just prior to deaih and usually die on their backs 

Diagnosis — symptoms, postmortem findings 

Cause — unknown, possibly related to nutritional deficiency 

Transmission — unknown 

Prevention — provide proper nutrition 

Treatment' — none 

Human Health Risk — none known 
Roup. See Canker, Cholera (chronic), Infectious Coryza, Roup (nutritional) 
Roup (nutritional) 

Also Called — A-avitaminosis 

Incidence — rare except when homemade rations are fed 
System/Organ Affected — upper respiratory (eyes, nose, throat) 
Progression — chronic 

Symptoms — in chicks 1 to 7 weeks old: droopiness, pale combs, and failure to 
grow followed by sore, swollen eyelids, sticky or cheesy discharge from eyes 
and nostrils, swollen sinuses, difficulty breathing 

— in hens: unthriftiness and decreased egg production followed by runny 
eyes and nose, eyelids stuck together, ruffled feathers, whitish-yellow mouth 
sores in severe cases, weakness, emaciation, increased interval between 
clutches, increased blood spots 

Percentage Affected — high 

Mortality — up to 1 00 percent 

Postmortem Findings — dry. dull respiratory lining; excess urates in cloaca! bursa 
Resembles — cholera (chronic), chronic respiratory disease, infectious bronchitis, 

infectious coryza, influenza 
Diagnosis — symptoms, postmortem findings, microscopic examination of body 

tissue, ration evaluation 
Cvuse — vitamin A deficiency for 2 to 5 months; chicks hatched from deficient 
breeders will be deficient unless fed fortified starter ration 
i — does not spread from bird to bird 
n — use only fresh feed (buy small quantities so it won't go stale); allow 
birds to free range or feed them good sources of vitamin A such as new yellow 
(not white) corn and alfalfa meal 
Treatment — water-soluble vitamin A supplement in drinking water; vitamin A 

injections in severe cases 
Human Health Risk — none 
Hunting Syndrome 

Incidence — rare, occurs in Australia, Israel, Japan, and southeastern United States 

Slipped Tendon 303 

Systhm /Organ Asfbgted — entire foody 

Symptoms — in birds 4 to 10 weeks, after receiving contaminated vaccine as day- 
old chicks: poor growth, abnormal feathering (barbules compress against the 
shaft for a short distance); sometimes paralysis 

— in naturally infected birds of all ages: no symptoms 
POSTMORTEM Findings — sometimes enlarged nerves; atrophy of cloacal bursa 
Resembles — Marek's disease, except that run ting syndrome involves nerves to a 
lesser extent; infectious anemia, infectious bursal disease, infectious stunting 
syndrome (a different disease sometimes also called "broiler runting syn- 

Diagnosis — flock history (use of polentially contaminated vaccine), symptoms. 

postmortem findings, laboratory identification of virus 
Cause — retrovirus that affects a variety of birds accidentally introduced lo 

chickens through vaccines contaminated during manufacture 
Transmission — contact with infected birds, their body fluids, or droppings; 

occasionally spread from breeders (cocks as well as hens) through hatching 

eggs; possibly spread by mosquitoes and other insects 
Prevention — none known; insect control and good sanitation help 
Treatment — none known 
Human Health Risk — none known 


Salmonella enteritidis. See Paratyphoid 

Salmonellosis. SeeArizonosis, Typhoid, Paratyphoid, Pullorum 
Sinusitis. See Chronic Respiratory Disease 
Slipped Tendon 

Also Called — chondrodystrophy, perosis 
Incidence — common in heavy, fast-growing breeds 
System / Organ Affected — hock 

Symptoms — in young birds, starting at 9 days ol age: swollen, flat hock joint; 
hopping on one leg, sometimes one or both legs twist or rotate to the side; 
death due to inability to obtain food and 

Percentage Affected — 3 to 5 percent 
Mortality — low 

Postmortem Findings — sometimes shortened, 

thickened long bones of legs and wings 
Resembles — twisted leg, except thai in twisted 

leg the bones are not shortened 
Diagnosis — history (birds' age, size, breed), 

symptoms, postmortem findings, ration 


B vitamins (biotin, choline, folic acid, Typical case of slipped tendon 

304 Sod Disease 

nicotinic acid, pyridoxine) 
Transmission — nutrilionaJ, does not spread from bird lo bird 
PREVENTION — breeil for genetic resistance; feed at least 95 percent commercial 
ration (no more than 5 percent corn or other treats); avoid crowding young 
birds; brood on litter rather than on slats, wire, or slick floor 

damage bin will minimize future damage 

Human Health Risk — none 
Sod Disease. Seefcrgotism 
Sore Head. See Pox (dry) 
Sour Crop. See Thrush 
Spirochetosis CALLED — fowl spirochetosis 

Incidence — common in free-ranged flocks in tropical and temperate climates, 
rare in North America (although the fowl tick that carries it is found in the 
south western United States) 

System /Organ AFFECTED — entire body (septicemic) 

Incubation Period— 3 to 12 days 

Progression — acute or chronic 

SYMPTOMS — in birds of all ages: droopiness, ruffled feathers, huddling, yellow 
green diarrhea with large amounts of white urates, increased thirst, loss of 
appetite, weak legs, pale or purplish comb, incoordination, loss of interest in 
perching, lying with head on ground, convulsions, fever, paralysis, drop in 
temperature to below normal just before death 

Percentage Aeiecied — I to 2 percent in carrier flocks with immunity due to 
constant exposure to ticks, up to 100 percent in susceptible birds mingled with 
immune birds 

Mortality — usually no more than 75 percent, but can be up to 100 percent 
Postmortem Findings — swollen, mottied spleen; sometimes greenish mucus in 

intestines, enlarged, spotted liver, swollen, pale kidneys and/or enlarged, pale 


RESEMBLES — influenza or Newcastle, excep! diat spirochetosis does not cause 
respiratory symptoms and bloody intestines; Marek's disease, except that 
spirochetosis does not produce tumors; cholera, typhoid, and septicemic 
colibacillosis, except that in spirochetosis Salmonella, Pasleurella, or E. colt 
bacieria cannot be found by laboratory 

Diagnosis — flock history (presence of fowl ticks, Argus persiciis), symptoms, 
postmonem findings, ideniification of spirochetes 

Cause — Bonelia aiiserina bacteria thai affect many birds but do not survive long 
in the environment 

Transmission — contact with moist droppings, blood, tissue, and mucus of 
Infected birds; spread by eating or being bitten by an infective fowl tick, 
mosquito, or other bloodsucker; spread through cannibalism (including 
picking carcasses of dead infected birds), contaminated droppings in feed or 
water, using the same needle for flockwide inoculation, vaccination, or blood 

Sternal Bursitis 305 

Prevention — control ticks and other bloodsucking insects; do not combine tick- 
infested and susceptible birds; do not house clean birds where outbreak has 
occurred within 3 years; vaccine not available in the United States 

Treatment — none effective; inject individual birds with 20 mg oxytetracycline 
(intramuscular) once a day for 2 days or add I gram oxyletracycline per gallon 
of drinking water for 3 days; survivors are immune and are not carriers; treat 
only under supervision, this is a reportable disease, see "Reportable Diseases" 

of a related tick-borne spirochete, B. burgdorferi, which causes Lyme disease in 
both birds and humans) 

Spondylolisthesis. See Kinky Back 
Staphylococcic Arthritis 

Also Called — arthritis/synovitis, staphylococcic septicemia 
Incidence — common worldwide 

System/Organ Affected — joints or entire body (septicemic) 

Incubation Period — 2 to 3 days (septicemic, form) 

Progression — acute (septicemic form) or chronic (arthritic form) 

Symitoms — in all ages (most often growing birds): fever, reluctance to move, 

ruffled feathers, depression, swollen joints (hot to the touch), resting on hocks 

and keel, lameness (chronic), death (acute) 
Percentage Affected— low 
Mortality — low 

Postmortem Findings — joints (especially hock) and surrounding area are 
inflamed and contain whitish, fleck-rilled pus that appears cheesy in an 
advanced infection; sometimes swollen, spotted liver and spleen 

Resembles — in young birds: joint infections (synovitis) caused by other bacteria; 
viral arthritis, except that in viral arthritis fluid surrounding joints is yellowish 
or pinkish 

— in mature birds: acute cholera (septicemic form), except that cholera 
involves a greater number of deaths 
Diagnosis — symptoms, laboratory identification of bacteria 
Cause — Staphylococcus aureus bacteria common in the poultry environment 
Transmission — bacteria entering body through wounds 
Prevention — prevent injuries by providing safe, uncrowded bousing 
Treatment — staph bacteria are resistant to many antibiotics, but treatment may 
be successful if a suitable antibiotic is determined through laboratory sensitiv- 
ity testing 

Human Health Risk — unsanitary handling of meat during or following butcher- 
ing can cause food poisoning in humans; see "Staphylococcal Food Poisoning" 
page 243 

Staphylococcic Septicemia. See Staphylococcic Arthritis 

Star-Gazing Syndrome. See Epidemic Tremor 
Sternal Bursitis. Sec Breast Blister 

306 Stomatitis 

Stomatitis. See Thrush 
Streptococcosis. (See also Omphalitis) 

Incidence — worldwide but not common 

System/Organ Affected — entire body (septicemic) 

Incuration Period — 5 to 21 clays 

Progression — acute (septicemic) or chronic 

Symptoms — in mature birds: depression, weight loss; sometimes lameness, head 
tremors, yellow diarrhea, pale combs and wattles, fever (108-1 10T, 42-43°C), 
eventual or sudden death 

Percentage Affected — up to 50 percent 

Mortality — up to 50 percent 

Postmortem Findings —enlarged, pale heart; light-colored or dark red patchy 
areas on liver 

Resembles — septicemic tonus of staphylococcosis, colibacillosis, pasteurellosis. 

erysipelas, otiier bacterial diseases 
Diagnosis — symptoms and laboratory identification of bacteria 
Cause — Streptococcus zooepidemiciisbactcria that normally live in a chicken's 

intestines; infection is considered secondary, since it occurs only if resistance 

is reduced by some other disease 
Transmission — inhalation, ingestion, skin wounds; bacteria are extremely 

susceptible to drying and so cannot be spread on equipment 
Prevention — practice good sanitation; avoid stress 

Treatment — bacteria are resistant to many antibiotics, but treatment mm' reduce 

sensitivity testing 
Human Health Risk — none known 
Stress Disease. See Chronic Respiratory Disease 
Stunting Syndrome. See Infectious Stunting Syndrome 
Sudden Death Syndrome 

Also Called — SDS, acute death syndrome, ADS, acute heart failure, fatal 

syncope, flip-over disease, heart attack ("sudden death syndrome" in maturing 
broiler breeders in Australia is caused by an unrelated nutritional deficiency) 
Incidence — common worldwide, especially in intensively managed broilers 
System/Organ Affected — heart and lungs 
Incubation Period — days to weeks 
Progression — acute 

Symptoms — in apparently healthy broilers, 1 to 12 weeks of age, primarily cocks: 
extended neck, gasping or squawking, wing beating, leg pumping, flipping 
onto back, death within 1 minute of first symptoms 

— in laying hens: cloacal tissue protrudes through vent, death 

Percentage Affected — up to 5 percent 

Mortality — 100 percent 

Postmortem Findings — feed-filled intestine; bloated, bright red lungs; pools of 
fluid between ribs and lungs; empty gall bladder; sometimes motded muscles, 
liver, and kidneys; 

Thick Leg Disease 307 

— in hens: numerous blood vessels covering egg yolk cluster, sometimes 

internal broken -shelled egg 
Resembles — round heart disease, except in sudden death syndrome birds go into 

convulsions before dying 
Diagnosis — symptoms, postmortem findings 

Cause — unknown; may be caused by high carbohydrate feeds and rapid weight 

gain relative to feed intake 
Transmission — nutritional, does not spread from bird to bird; do not feed for 

rapid weight gain 

Prevention — low-intensity lighting; avoid noise and other disturbances 

Treatment — none 

Human Health Risk — none known 
Summer Disease. SeeBluecomb 
Swollen Head Syndrome 

Also Called — dikkop. facial cellulitis, SHS, thick head 

Incidence — not found in North America; prevalent in Israel, South Africa, and 
parts of Europe 

System/Organ Affected — head 

Incubation Period — 36 hours 

Progression — spreads rapidly 

Symptoms — in broilers and broiler breeders: sneezing, red swollen eyes, progres- 
sive swelling of the head and wattles, scratching of face with feet, drop in egg 
production; sometimes nervous symptoms; death 

Percentage Affected — less than 4 percent 

Mortality — 4 to 10 percent 

Postmortem Findings — inflamed pus-filled tissue beneath the skin of head 

Resembles — infectious bronchitis, infectious coryza, Newcastle 

Diagnosis — Hock history (contact with infected turkeys), symptoms, laboratory 

Cause — combination of Escherichia coli and possib 

follows debeakhg or vaccination for Newcastle 
Transmission — contact with turkeys infected with turkey coryza (rhinotracheitis) 

or drinking water contaminated widi the virus 
Prevention — provide adequate ventilation; avoid crowding; practice good 

sanitation and litter management; avoid mixing birds of different ages or 

r — improve ventilation; keep birds warm and well fed with high protein 
rations £ 

Human Health Risk — none known 
Synovitis. See Infectious Synovitis 


Tenosynovitis. See Viral Arthritis 
Thick Leg Disease. See Osteopetrosis 

308 Thrush 


Also Called — candidiasis, crop mycosis, moniliasis, muguet, oidica, 

oidiomycosis, sour crop, stomatitis 
Incidence — common 

System/Organ Affected — upper digestive tract 
Incubation Period — 2 to 4 weeks 
Progression — chronic 

Symptoms — in growing birds: depression, rough feathers, diarrhea, distended 

sour crop, slow growth or weight loss 
Percen tage Affected — up to 20 percent 
Mortality — up to 5 percent 

Postmortem Findings — grayish white, rough, circular, thickenings that join to 
create a "Turkish towel" appearance in mouth, esophagus, and crop lining, 
sometimes in stomach, rarely in the intestine 

Resembles — canker, capillary worms, pox (wet) 

Diagnosis — flock history (age of birds, outbreak of coccidiosis or use of antibiot- 
ics), symptoms (unthrifty birds), postmortem findings 

Cause — Candida albicans yeasi-like fungus commonly living in the bowels of 
chickens that infect when normal flora are disrupted by coccidiosis or antibiot- 
ics, growth promoters, and other drugs; sometimes found in connection with 
another disease (especially coccidiosis or chJamydiosis) 

Transmission — contaminated droppings in drinking water 

Prevention — good nutrition and sanitation; avoid parasites; clean feeders and 
waterers regularly; avoid crowding; avoid prolonged treatment with antibiotics 
and other drugs 

Treatment — isolate infected birds; clean and disinfect feeders and waterers; flush 
with molasses or Epsom salts (see "Flushes," page 192), followed by Vz tea- 
spoon copper sulfate (powdered bluestone) per gallon drinking water every 
other day for 5 days served in a r - 
mouth sores with an antiseptic such as 1 

Human Health Risk — C. albicans can cause mouth and genital infection in 
humans, see "Candidiasis" page 232 
Tibial Rotation. See Twisted Leg 
Toxicoinfection. See Botulism 


Also Called — toxoplasma 

Incidence — worldwide but sporadic and rare 

) — central nervous system; sometimes reproductive 
I organs 

Incubation Period — 3 to 12 days 

Progression — usually acute in young birds, chronic in older birds 
Symptoms — primarily in young, stressed birds: loss of appetite, emaciation, pale, 
shriveled comb, white droppings; sometimes diarrhea, incoordination, 
walking in circles with head twisted back, muscle spasms, paralysis, blindness; 

Tuberculosis 309 

lasts as long as 3 weeks, often ends in death 
Percentage Affected — high 
Mortality — up to 50 percent 

Postmortem Findings — enlarged, mottled liver; blood-filled lungs 
Resembles — Marek's disease, Newcastle, or any other infection involving the 

Diagnosis — laboratory identification of protozoa 
Cause — Toxoplasma gondii protozoan parasite 

Transmission — picking in infected droppings of housecats or related animals, 
picking at infected meal (including infected chickens, dead or live), eating 
infected earthworms, eating flies or cockroaches carrying toxoplasma on their 

Prevention — control flies, cockroaches, dung beetles, rodents 
Treatment — none known 

Human Health Risk — eating undercooked meat contaminated with infected 
droppings can (though rarely does) cause infection in humans, see 
"Toxoplasmosis" page 235 
Trichomoniasis. See Canker 
Trichothecene Mycotoxicosis. SeeFusariotoxicosis 

Also Called — avian tuberculosis, AT, TB 

Incidence — common worldwide, especially in backyard flocks in temperate 

northern climates (northcentral United States) 
System/Organ Affected — starts in intestinal tract and migrates to other internal 

Incubation Period— years 

Progression — usually chronic, rarely acute, spreads very slowly 
Symptoms — in birds 2 years old or older (especially living in contact with soil): 
dull, ruffled feathers, gradual weight loss despite good appetite, shrunken 
breast muscles, prominent (often deformed) keel; persistent diarrhea, pale 
(sometimes bluish) combs and wattles, decrease in laying; sometimes lame- 

Percentage Affected — 10 to 50 percent, spread over many months 
Mortality — 100 percent 

liver, spleen, intestine, and bone marrow, increasing in size and number with 
the length of time the bird is infected 

RESEMBLES — blackhead, except that in blackhead organ spots are dished rather 
than knobby; avian leukosis complex, except that leukosis usually affects 
younger birds; air-sac mites, which can be detected only by seeing tiny 
translucent dots moving around in air sacs soon after bird dies (see page 71) 

Diagnosis — flock history (bird's age, chronic disease conditions), symptoms 
(extreme emaciation, continuing deaths), postmortem findings, laboratory 

birds may be skin tested byusinga 1 ml tuberculin syringe and '/2-inch (1.3 

310 Twisted Leg 

cm), 26 gauge needle to inject 0.05 ml avian tuberculin into wattle skin; 

swelling after 48 hours indicates test is positive, although infected birds 

occasionally react negatively 
Cause — Mycobacterium avium bacteria that survive for 6 months or more in litter 

and up to 4 years in soil, affect a wide variety of birds 
Transmission — droppings of infected birds or picking ai contaminated carcasses 

of dead birds; spread on contaminated shoes and equipment 
Prevention — do not keep chickens over 18 months old; do not mix birds from 

different age groups; design housing so birds can't pick in droppings; rotate 

'range; remove reactors to wattle test 
Treatment — none effective, cull; thoroughly clean and disinfect housing with a 

cresylic compound, remove the top 4 inches of soil in dirt-floor housing and 

replace it with uncontaminated soil; remove 2 inches of range topsoil or keep 

new birds off contaminated range for at least 4 years 
Human Health Risk — M. avium is not the same bacterium that normally causes 

human TB; human infection is rare but possible in people who have been 

sensitized to human or bovine TB or who have acquired immune deficiency 

Twisted Leg 

Also Called — crooked legs, long-bone distortion, tibial rotation, valgus leg 

deformity, valgus or varus deformation, WD, windswept 
Incidence — common in battery-raised broilers 
System/Organ Affected — long bones of leg 
Progression — rapid onset (1 to 2 days) 

Symptoms — in broilers 1 week of age and older, primarily cockerels: one or both 
legs bend outward at hock joints by as much as 90°, sometimes with a pointed 

protrusion at the hock joint; sometimes birds 
walk on bruised, swollen hocks 
Percentage Affected — up to 2 percent in mixed 
flocks, up to 25 percent in all-cockerel flocks; 
highest in birds brooded on wire 
Mortality — none 

Postmortem Findings — outward or inward 

angulation of upper or lower bones 
Resembles — slipped tendon, except that twisted 

leg bones are not widened and shortened 
Diagnosis — symptoms 
Cause — unknown, may be genetic or nutri- 
tional; possibly related to slipped tendon 
Transmission — unknown 
Prevention — raise broilers on litter (rather than 

on wire) and do not feed for rapid growth 
Treatmeni — none, condition is not reversible 
Twisted leg Human Health Rjsk - none known 

Ulcerative Enteritis 311 


Also Called — fowl typhoid, FT, infectious leukemia (one kind of salmonellosis) 

Incidence — worldwide, rare in North America 

System/Organ Affected — digestive or system wide (septicemic) 

Incubation Period — 4 to 5 days 

Progression — usually acute, running through flock in about 5 days, sometimes 

Symptoms — in chicks: sudden death soon after hatching or loss of appetite, 
sleepiness, weakness, droopy wings and head, labored breathing, increased 

— in growing birds over 12 weeks old (most common group affected): 
sudden loss of appetite, droopiness, ruffled feathers, huddling near heal, pale 
heads, shrunken combs, temperature 1 to 5 "F {1 to 3"C) above normal, 

— in mature bird: depression, ruffled feathers; sometimes pale heads, 
increased thirst, dehydration, shrunken combs, greenish or yellowish diarrhea 

Percentage Affected — varies widely 
Mortality — in chicks: up to 90 percent 

— in growing and mature birds: 10 to 50 percent 
Postmortem Findincs — in young birds: swollen, red liver, spleen, and kidneys 

— in older birds: dark, swollen green or bronze liver, sometimes with gray 
spots; enlarged, sometimes mottled spleen; swollen kidneys; slimy, inflamed 
intestines; brownish lungs; thin, watery blood 

Resembles — paratyphoid and pullonim, except that typhoid often continues for 
months, usually affects older birds, and causes higher mortality 

Diagnosis — flock history, symptoms, postmortem findings, laboratory identifica- 
tion of bacteria 

Cause — Salmonella gallinantm bacteria that affect turkeys as well as chickens 
and survive for 6 months or more in litter and soil 

Transmission — from infected breeders to chicks through hatching eggs; contami- 
nated litter, equipment, shoes, flies, feet of animals and wild birds 

Prevention — purchase certified typhoid-free stock; blood test birds and elimi- 
nate carriers; clean and disinfect regularly; control Hies, rodents, animals, and 
wild birds; keep chickens away from contaminated ponds and other surface 
water; rotate range-fed flock; chickens raised in areas where typhoid is 
prevalent tend to develop resistance 

Treatment — not recommended, survivors are carriers; this is a reportable 
disease in most states, see "Reportable Diseases" page 196 

Human Health Risk — none known, not the same disease as typhoid fever in 


Ulcerative Enteritis 

Also Called— quail disease, UE 
Incidence— common worldwide 

312 Urolithiasis 

System/Ohcan Affected — digestive (lower intestine and ceca) 
Incubation PERIOD — 1 to 3 days 

Progression — acute or chronic, runs its course in 2 to 3 weeks 
Symptoms — in young birds, 4 to 1 2 weeks old (commonly 5 to 7 wee<s): sudden 
death with no symptoms; or listlessness, dull, ruffled feathers, hunched-up 
posture with head pulled in and eyes closed, diarrhea (sometimes bloody), 
extreme emaciation, death within 2 to 3 weeks 
Percentage Affected — low 

Mortality — less Uian 1 percent, peaking within a week 
Posi-moktem Findings — yellowish button-like dots (ulceraiions) throughoul 
intestinal tract, concentrating in lower intestine and cecum; patchy tan or 
yellow areas on liver; enlarged, mottled spleen; shriveled breast muscle 
Resembles — blackhead, except that blackhead does not involve the spleen or 
lower intestine; coccidiosis, except thai cocci often causes bloody droppings 

or ceca 

Diagnosis — symptoms, postmortem findings (buttons in intestine, colorful 
patchy liver) 

Cause — Clostridium colinum bacteria that affect game birds more often dian 
chickens, persist under varying conditions (hot, cold, dry, humid), and resist 
disinfectants; often occurs in combination with coccidiosis, myccplasniosis, or 
parasites (internal or external); often follows infectious anemia or infectious 
bursal disease; outbreak results in permanent contamination of housing 

Transmission — contagious; spreads in droppings of infected or carrier birds 
picked from litter, feed, or water; spread by Hies 

Prevention — in problem areas, remove and replace litter between flocks or raise 
birds on wire; avoid crowding; manage flock to avoid coccidiosis, internal and 
externa] parasites, and viral diseases (all of which reduce resistance); do not 
combine birds of different ages or from different sources 

Treatment — streptomycin in drinking water at the rate of 15 grams per gallon for 
10 days, then 1 gram per gallon for 5 more days; remove old litter; natural 
survivors are resistant, treated survivors remain susceptible, all survivors may 
be carriers 

Human Health Risk — none known 
Urolithiasis. See Gout (visceral) 
Uveitis. SeeMareks Disease 


Valgus Leg Deformity. See Twisted Leg 

Valgus or Varus Deformation (WD). See Twisted Leg 

Velogenic Newcastle. See Newcasde Disease (exotic) 

Vent Gleet. See Pasted Vent 

Vesicular Dermatitis. See Ergotism 

Viral Arthritis 

Also Called — arthritis/ tenosynovitis, reovirus infection, ruptured tendon 
Incidence — worldwide but rare 
System/Organ Affected — joints and tendons 
Incubation PERIOD — 1 to 13 days 
Progression — acute or chronic 

Symptoms — in young birds (primarily heavy breeds) 4 to 16 weeks old: lameness, 
stunted growth, uneven gait, swollen hocks, foot, and other joints 

Percentage Affected — nearly 100 percent 

Mortality — 2 to 10 percent, primarily in young birds 

Postmortem Findings - 

yellowish or pinkish sticky fluid 

Resembles — staphylococcic arthritis, except that in staph arthritis fluid surround- 
ing joints is whitish and contains flecks; simple leg injury, except that injury 
involves only individual birds 

Diagnosis — flock history (age of birds), symptoms (both shanks swollen), 
confirmed by laboratory identification of virus 

Cause — avian reovirus that infects only chickens 

Transmission — contact with infected birds and their droppings or respiratory 
discharges; spreads from breeders to chicks through hatching eggs 

Prevention — avoid crowding; do not hatch eggs from infected breeders; vacci- 
nate breeder flock to pass parental immunity to chicks; chicks start developing 
natural immunity by 2 weeks of age 

Treatment — none; mildly infected birds recover in 4 to 6 weeks; cull severely 
affected birds, as they rarely recover; following an outbreak, thoroughly clean 
and disinfect housing with lye or 0.5 percent organic iodine solution 

Human Health Risk — none 
Visceral Lymphoma. Sep Lymphoid Leukosis 
Visceral Urate Deposition. See Gout (visceral) 

Viscerotropic Velogenic Newcastle Disease. See Newcastle Disease (exotic) 
Vitamin A Deficiency. See Roup (nutritional) 

Vitamin E Deficiency. See Encephalomalacia, Exudative Diadiesis, White Muscle 


Water Belly. See Broiler Ascites 
Western Duck Sickness. See Botulism 
Wet pox. See Pox (wet) 
White Comb. See Favus 
White Diarrhea. SeePullorum 
White Muscle Disease 

Also Called — muscular dystrophy, nutritional myopathy 

Incidence — not common 

314 Windpuff 

System/Organ Affected — muscles 

Symptoms — in chicks 4 weeks old: degeneration of breast and sometimes leg 

Percentage Affected — 10 to 15 percent until diet is corrected 
Mortality — low 

Postmortem Findings— yellow to grayish white streaks (degenerated muscle 

fibers) in leg or breast muscle 
Diagnosis — symptoms, postmortem Findings, ration evaluation, absence of 


Cause — deficiency of vitamin E and selenium 

Transmission — nutritional problem, does not spread from bird to bird 
Prevention — use only fresh commercial rations fortified with Vitamin E and 
selenium; store feed in cool, dry place and use within 2 weeks of purchase 
Treatment — vitamin E supplement by injection, in feed, or orally (300 IU per 

bird); replace old feed; with proper treatment, condition is reversible 
Human Health Risk — none 
Windpuff. See Emphysema 
Windswept. See Twisted Leg 
Wing Rot. See Necrotic Dermatitis 


X Disease. SeeAflatoxicosis, Bluecomb 

- Y - 

Yolk Sac Infection. SeeColibacillosis, Omphalitis 


The following words are defined in the context of chicken health. In another 
con text some words may have other or broader meanings. 

Abscess. Pocket filled with pus. 
Acariasis. Mite infestation. 

Acute. Having a severe and short development, often measured in hours and 

ending in death or recovery; opposite of chronic. 
Anemia. Deficiency of the blood in quantity or quality due to blood loss or 

disease, characterized by weakness and pale skin. 
Anthelmintic. VVormer. 

Antibiotic. A soluble chemical produced by a microorganism or fungus and 
used to destroy or inhibit the growth of bacteria and other microorgan- 

Antibody. A natural substance in the blood that recognizes and destroys 
foreign invaders and that causes an immune response to vaccination or 

Antigen. A foreign protein that differs from natural body proteins and 
therefore stimulates the production of antibodies. 

Antiseptic. Anything that destroys or inhibits microorganisms responsible 
for disease, decomposition, or fermentation. 

Antitoxin. An antibody thai neutralizes toxins produced by bacteria. 

Arthritis. Inflammation of the joint and surrounding tissue. 

Ascaridiasis. Roundworm infection. 

Ascites. Accumulation of fluid in the abdominal cavity. 

Atrophy. Shrinking or wasting away of a body part. 

Attenuated. Weakened so as not to produce disease but still induce immu- 
nity when used as vaccine (said of viruses). 

Avian. Pertaining to birds. 

Bacteria. Microscopic, single-celled plants that may or may not produce 

disease (singular: bacterium). 
Bactericide. A substance that kills bacteria. 
Bacterin. A vaccine produced from bacteria or their products. 
Bacteriostat. A substance that inhibits or retards bacterial growth. 
Ballooning. Distention of the intestine or ceca due to accumulated blood, 

mucus, or other materials. 
Benign. Not likely to recur or spread. 
Biosecurity. Disease-prevention management. 


316 Tub Chicken Umm Handbook 

Blow-out. Venl damage due to laying an oversized egg. 
Booster. Vaccination other than the first in a series. 
Bursa of Fabricius. Cloacal bursa. 
Cannibalism. Eating one's own kind. 
Cancer. Malignant tumor that lends to spread. 

Cankers. Whitish bumps that erupt to form sores, usually on the face or in 

the mouth. 
Capillariasis. Capillary worm infection. 

Carrier. An apparently healthy individual that transmits disease-causing 

organisms to other individuals. 
Cauterize. To use a hot iron to burn, sear, or destroy tissue. 
Cecum. A blind poucli at the juncture of the small and large intestine that 

resembles the human appendix (plural: ceca). 
Cephalic. Pertaining to the head or skull. 
Cestode. Tapeworm. 
Cestodiasis. Tapeworm infection. 
Chondrodystrophy. Having short bones. 

Chromosome. Microscopic cell containing the genes that carry hereditary 

Chronic. Having long duration measured in days, months, or even years and 
being somewhat resistani to treatment; opposite of acute. 

Clinical. Having signs or symptoms that can be readily observed. 

Cloaca. The lower end of the digestive tract where the digestive, reproduc- 
tive, and excretoiy tracts come together. 

Clubbed down. Down that fails to emerge in an embryo or newly hatched 
chick, most commonly around neck and vent. 

Coccidiasis. Infection with coccidial protozoa without showing any signs. 

Coccidiosis. Infection with coccidial protozoa. 

Coccidiostat. A chemical added at low levels to feed or water to prevent 

Cockerel. A male chicken under 1 year of age. 
Coliform. Any bacteria resembling Escherichia coli bacteria. 
Congested. Filled with blood. 

Conjunctiva. Mucous membrane covering the eyeball and inner surface of 
the eyelid. 

Conjunctivitis. Inflammation of the conjunctiva. 

Contagious. Readily transmitted from one individual or flock to another. 
Crop. To surgically remove wattles; also, the pouch at the base of a bird's 

neck where feed is temporarily stored. 
Cull. To kill a diseased or otherwise unproductive bird. 
Culture. To incubate a sample from a diseased bird for several hours (or 

Glossary 317 

days) and look for the presence of bac terial growth. 
Cyst. A sack-like structure containing fluid or semi-solid material. 
Debeak. To trim back the top beak to prevent cannibalism. 
Dehydration. Loss of body water (over 12 percent loss results in death). 
Depopulate. Get rid of an entire flock. 
Dermatitis. Inflammation of the skin. 
Diarrhea. Frequent, runny bowel movements. 
Diathesis. Susceptibility to certain diseases. 

Disease. Any departure from normal health or impairment or normal body 
functions. ^ 

bird's body. 

Drench. To give liquid medication orally (by mouth); also the liquid medica- 
tion itself. 

Dub. To surgically remove a bird's comb. 

Duodenal Loop. Upper small intestine (same as "duodenum"). 

Ectoparasite. External parasite. 

Edema. Accumulation of excessive fluid in swollen or damaged tissues. 
Electrolyte. Natural chemical in the blood needed by body cells to maintain 

balance; also, mineral solution used to treat dehydration. 
Emaciation. Wasting away of the body. 
Embryo. A developing chick within an egg. 

Embryonation. Development of an embryo into a larva inside an egg 

without hatching. 
Encephalitis. Inflammation of the brain. 
Endoparasite. Internal parasite. 
Enteric. Affecting the intestines. 
Enteritis. Inflammation of the intestine. 
Enteropathogens. Microbes that cause enteritis. 
Enterotoxin. A substance that poisons cells lining the intestines. 
Enzootic. The continuing presence of a disease or infectious agent in a 

specific area (equivalent to "endemic" human diseases). 
Epizootic. Epidemic among chickens or other animals (similar to the word 

"epidemic" pertaining to humans). 
Esophagus. Channel that moves food from the throat to the stomach. 
Etiology. The study of causes of diseases. 
Eversion. Turned inside out. 

Exudate. Fluid associated with inflammation or swelling. 

Exudative diathesis. Accumulation of fluid (exudate) under die skin or 

around the heart. 
Fecal. Pertaining to feces. 
Feces. Droppings or body waste. 

318 THE Chicken Health Handbook 

Flaccid. Limp. 

Fluke. Trematode flatworm parasite. 

Fomites. Inanimate objects such as shipping crates, feed sacks, clothing, and 
shoe soles that may harbor disease-causing organisms and may be either 
a vehicle or a reseivoir of infection. 

Fungus. A plant that does not contain chlorophyll and that reproduces 
through spores (plural: fungi). 

Genes. Parts of chromosomes diat carry hereditar y factors. 

Genetic. Pertaining to genes. 

Germs, Disease-causing microbes. 


Going light. Growing thin while eating rave 
Gross. Can be seen with the naked eye. 
Gross lesions. Easily observable changes in tissues or organs. 
Helminth. A category of par asitic worms. 
Helminthiasis. Parasitic worm infestation. 
Hemorrhage. Heavy or uncontrolled bleeding. 
Hepatitis. Inflammation of the liver. 

Horizontal transmission. Transmitted from one bird to another. 
Host. A bird (or other animal) on or in which an infectious agent lives. 
Ileum. Lower small intestine. 
Immune. Resistant. 

Immunity. Resistance or ability to resist infection. 

Immunity, active. Resistance to a disease as a result of having had the 

Immunity, passive. Resistance to a disease as a result of injection with 

Immunoglobulin. Antigen. 
Impaction. Blockage of a body passage or cavity. 
Incidence. Number of cases of a particular disease diagnosed during a 

particular time period. 
Incubation period. The time it takes from exposure to a disease-causing 

agent until the first symptom appears; also, the time it takes for a bird's 

egg to hatch. 

Infection. The entry of an organism into a body and causing of disease by 

developing or multiplying therein. 
Infectious. Capable of invading living tissue and multiplying therein, 

causing disease. 
Infertility. Inability to reproduce. 

Inflammation. Reaction of tissue to injury or irritation, whereby it becomes 

red, hot, swollen, painful, and possibly loses its function. 
Ingest. Eat. 

Glossary 319 

Initial vaccination. First vaccination in a series. 
Inoculate. To give an injection. 
Inoculant. A substance tliat*s injected. 

Intraocular. In the eye. 
Intranasal. In the nose. 

Immunosuppressant. Any cause of reduced disease resistance. 

Intravenous (IV). Placement of an injection into a vein. 

...itis. Suffix indicating inflammation (e.g. sinusitis means inflammation of 

the sinus cavities). 
IU. International Unit, in which some drugs are measured. 
Jejunum. Middle small intestine. 
Joint ill. Arthritis. 
Laceration. Jagged wound. 

Lesion. A change in size, shape, color, or structure of an internal organ. 
Leukosis. A disease of the blood-forming organs. 

Lymphatic system. Circulating system that contains the immune system's 

Metabolism. All the physical and chemical processes diat produce and 

maintain a living body. 
Metastasis. The transfer of disease from one organ to another that it isn't 

directly touching. 
Metastasize. Spread to other tissues or organs. 
Microscopic. Cannot be seen by the naked eye. 
Mite. A small to microscopic jointed-legged creature. 
Mold. A type of fungus. 

Molt. Natural shedding and renewal of feathers. 
Morbid. Having or causing a disease. 
Morbidity. Percentage affected by disease. 

a given time period. 
Moribund. Dying. 
Mortality. Death rate. 

Mortality rate. The number of birds in a flock that die from a disease within a 

given time period. 
Mucous membrane. The lining of body cavities. 

chemical processes. 

The numl 

320 The Chicken Health Handbook 

Mucus. Slimy substance produced by mucous membranes. 
Mycosis. Any disease caused by a fungus. 
Myopadiy. Any disease of the muscles. 

Necropsy. A postmortem examination (equivalent to a human autopsy). 
Necrotic. Pertaining to dead tissue. 

Necrotic enteritis. Inflammation and decaying of intestinal tissue. 

Nematode. Roundworm. 

Neoplasm. A tumor or other abnormal growth. 

Nephrids. Inflammation of die kidneys. 

Neural. Pertaining to nerves. 

Noninfectious disease. A disease that is not caused by a biological organism. 
Noxious. Unpleasant. 
Ocular. Pertaining to the eye. 

Oocyst. The infective fertilized egg of certain one-celled animal parasites. 
Opportunistic. A microorganism that is non-infectious to healthy birds; 

infectious only to birds with reduced resistance from some other cause. 
Organism. A living thing. 

Osteomyelitis. Inflammation of the bone marrow. 
Osteopetrosis. Increased size, density, and brittleness of the bone. 
Osteoporosis. Thinning and weakening of the bone. 

Oviduct. Channel through which an egg passes after it leaves a hen's ovary. 

Parasite. A living organism diat survives on another living organism withoul 
providing any benefit in return. 

Parental immunity. Resistance to disease passed from breeders to their 
offspring through the egg. 

Parenteral. Located outside the intestines, used in referring to drugs intro- 
duced by injection rather dian by mouth. 

Pasting. Loose droppings sticking to the vent area. 

Pathogen. Disease-producing organism or agent. 

Pathogenic. Capable of causing disease. 

Pathogenicity. Degree of ability to cause disease. 

Pathology. The study of damage caused by disease. 

Pathologist. A medical professional who looks for internal damage caused 
by disease. 

Pediculosis. Louse infestation. 

Peracute. Having extremely severe and short duration, measured in minutes 
or hours. 

Perosis. Malformation of the hock joint. 

pH. A number that indicates acidity or alkalinity; 7 is neutral, above 7 is 

alkaline, below 7 is acid. 
Pick-out. Vent damage due to cannibalism. 
Pneumonia. Any disease of the lungs. 

Glossary 321 

Popeye. Emaciation of chicks (causing eyes to appear large in relation to 

Post. To conduct a postmortem examination. 
Postmortem. Pertaining to or occurring after death. 
Predispose. To cause susceptibility to disease. 

Prevalence. The number of cases of a disease in a flock during a given time. 
Priming vaccination. Vaccination that increases antibody levels before 

another product is used to induce immunity. 
Prolapse. Slipping of a body part from its normal position, often used 

incorrectly to describe ail everted organ. 
Progeny test. Evaluation of breeders based on the performance of their 


Protective synergism. Phenomenon by which two vaccines confer greater 

protection than the sum of their individual effects. 
Protozoan. A single-celled microscopic animal that may be eitiier parasitic 

or beneficial (plural: protozoa). 
Proventriculus. A chicken's stomach, lying between the crop and the 


Pullet. A female chicken under one year of age. 
Purulent. Full of pus. 

Pus. Liquid, produced by inflammation, containing dead white blood cells. 

Rales. Ajw abnormal sound coming from the airways. 

Rattling. Abnormal sound coming from the throat. 

Reactor. A bird that reacts positively to a test for an infectious disease. 

Renal. Pertaining to the kidneys. 

Reportable. A disease that is so serious it must, by law. be reported to a state 

or federal veterinarian. 
Reservoir of infection. Any animate or inanimate object on which an 

infectious agent survives and multiplies and from which it can be 

transmitted to a susceptible host. 
Resistance. Immunity or ability to resist infection. 
Respiration rate. Number of cycles per minute by which air is moved into 

and out of the lungs. 
Rhinitis. Inflammation of the lining of the nasal passages. 
Rigor mortis. Stiffness following death. 

Roup. Any condition involving chronic infection of skull membranes. 

characterized by facial swelling. 
Salpingitis. Inflammation of the oviduct. 

Secondary infection. A disease that invades after a bird's immune defenses 

have been weakened by some other disease. 
Secretion. Fluid coming from a body organ. 
Seleniferous. High in selenium. 

Self-limiting. Any disease that runs its course in a specific amount of time 
then stops without treatment. 

Septicemia. Blood poisoning or invasion of die bloodstream by a micro- 

Serological. Pertaining to the testing of blood serum for antibodies against 
specific diseases. 

Serum. The clear liquid portion of the blood left after clotting (plural: sera). 
Sign. Objective evidence of disease consisting of symptoms and lesions. 
Sinus. A hollow space or cavity. 
Sinusitis. Inflammation of the sinus cavities. 

Spleen. Organ near the stomach that aids in the proper functioning of blood. 
Spore. The seed of fungi or the inactive form of certain bacteria, 
spp. (as in Salmonella spp.). More than one species. 
Starve-out. Failure of chicks to eat. 

Sterile. Entirely free of living organisms; also, permanently unable to repro- 

Sternum. Breastbone or keel. 

Stress. Any physical or mental disruption that lowers resistance. 
Subclinical. An inapparent infection for which signs or symptoms can be 

detected only through laboratory analysis. 
Subcutaneous. Directly beneath die skin. 
Symptom. Detectable evidence of disease. 

Syndrome. A group of symptoms that occur in combination in a particular 

disease, such as ranting syndrome. 
Synergistic. Working in cooperation (same as "synergetic"). 
Syringe. Tube with plunger that holds a drug to be injected. 
Systemic. Involving the entire body. 

Taeniasis. Obsolete word for cestodiasis (tapeworm infection). 
Tenosynovitis. Inflammation of the synovial shield of a tendon. 
Three-host dck. A tick that spends die three stages of its life on three differ- 
ent hosts. 
Torticollis. Twisted or wry neck. 

Toxemia. Generalized poisoning resulting from circulation through the body 

of toxins produced by bacteria. 
Toxin. A poison produced by microorganisms. 

Toxoid. An agent that confers immunity against toxins produced by bacteria. 
Trachea. Windpipe. 

Transovarian transmission. Infection of a hen's egg before the shell is 

Trauma. Wound or injury that destroys tissue. 

Traumatic ventriculitis. Piercing of die gizzard from the inside by a pointed 

Glossary 323 

Trematode. A fluke. 

Tubercle (as in tuberculosis). A tumor-like mass. 

Tumor. A mass of tissue that develops and grows without benefit to sur- 
rounding tissue. 
Ulcer. A raw, red sore. 

Unthrifty. Unhealthy appearing and/or failing to grow at a normal rate. 
Urates. Uric acid (salts found in urine), appearing as white crystals or paste. 
Uremia. Poisoning caused by accumulated wastes in the Body, usually due 

to kidney failure. 
Urolith. Urinary stone. 

Vaccine. Product made from disease-causing organisms and used to induce 

Vascular. Pertaining to blood ve 

source to another (examples: mosquitoes, ticks, flies). 
Vehicle. Anyt hing that mechanically carries disease from one place to 

another (examples: clothing, equipment, dust). 
Vent. The outside opening of the cloaca. 
Ventriculus. The gizzard. 

Venipuncture. Inserting a needle into the vein for the purpose of withdraw- 
ing blood. 

Vertebrae. Bones in the spinal column (singular: vertebra). 
Vertical transmission. Transmitted from parent to offspring through 
hatching eggs. 

Veterinary ethology. The study of animal behavior as it relates to health. 
Viremic. Of or pertaining to a virus in the blood. 
Viscera. Internal body organs and glands. 
Viscous. Thick and sticky. 

Virulence. Pathogenicity or ability to cause disease. 
Virus. An ultra-microscopic organism that multiplies only in living cells. 
Warfarin. An anti-coagulant used to poison rodents. 
Zoonosis. A disease transmissible from a chicken (or other animal) to a 
human (plural: zoonoses). 


American Livestock and Pet Supply. Inc. 

Madison, Wisconsin 

Cutler's Pheasant and Poultry Supply, 

Applegate, Michigan 


Double R Discount Pet, Poultry, and 
Avian Supply 

Palm Bay, Florida 


First State Veterinary Supply 

Salisbury, Maryland 
410-546-6137 ' 

G.Q.F. Manufacturing Company 

Savannah, Georgia 


Elemental Scientific, LLC 

(formerly Hagenow Laboratories, Inc.) 
Applcton, Wisconsin 

uumuu, auiu. 

Meyer Hatchery 
Polk, Ohio 

Murray McMurray Hatchery 

Webster City, Iowa 

www. mem uirayharchery. com 

Omaha Vaccine Company 

CSR Company Inc. 
Omaha, Nebraska 

PBS Animal Health 

Massillon, Ohio 

Lohmann Animal Health International 

Lampasas, Texas 


State Poultry Pathology Laboratories 


Alabama Veterinary Diagnostic 

Department of Agriculture & Industries 
Auburn, Boaz, Elba, and Hanceville, AL 


State Veterinarian 

Department of Environmental 


Anchorage, AK 




Arizona Veterinary Diagnostic 

University of Arizona 
Tucson, AZ 
520 621 2356 

http-.llm icrovet. arizona, edu/Az VDL 

Arkansas Livestock & Poultry 
Commission Veterinary Diagnostic 

Little Rock and Springdale, AR 



California Animal Health and Food 
Safety Laboratory System 

University of California, Davis 
Davis, San Bernardino, Tulare, and 
Turlock, CA 


Veterinary Diagnostic Laboratories 

Colorado State University 

Fort Collins. Grand function, and Rocky 

Ford, CO 



Connecticut Veterinary Medical 
Diagnostic Laboratory 

University of Connecticut 
Storrs, CT 


Poultry and Animal Health Section 

Delaware Department of Agriculture 

Dover, DE 


Bureau of Diagnostic Laboratories 

Florida Department of Agriculture & 
Consumer Services 
Kissimmee and Live Oak, FL 

Bureau of Laboratories 

Florida Department of Health 
Jacksonville, Lantana, Tampa, Miami, and 
Pensacola, FL 
www.doh.siate.fl. us/Lab 


Georgia Poultry Laboratory Network 

Camilla, Carnesville. Dalton, Forsyth. 
Glennville, and Oakwood, GA 

326 The Chicken Health Handbook 

Georgia Veterinary Diagnostic 

University of Georgia 
Athens and Tifton, GA 


Hawaii State Veterinary Laboratory 

Hawaii Department of Agriculture 


Animal Health Laboratory 

Idaho Slate Department of Agriculture 

Boise, ID 



Animal Disease Laboratories 

Illinois Department of Agriculture 
Cenlraiia and Galesburg, IL 


Indiana Animal Disease Diagnostic 

Purdue University 

West Lafayette and Dubois, IN 



Veterinary Diagnostic Laboratory 

Iowa State University 
Ames. IA 

Kansas State Veterinary Diagnostic 

Kansas Slate University 
Manhattan, KS 

Breathitt Veterinary Center 

Murray State University 
I lopkinsville, KY 

Veterinary Diagnostic Laboratory 

(formerly the Livestock Disease 
Diagnostic Center) 
University of Kentucky 
Lexington, KY 


Louisiana Animal Disease Diagnostic 

Louisiana State University 
Baton Rouge. LA 


Maine Veterinary Diagnostic Laboratory 

University of Maine 

Orono. ME 


www. umaine.edulveikib 


Animal Health Diagnostic Laboratories 

Department of Agriculture 

Annapolis, Frederick, and Salisbury. MD 



Division of Animal Health Poultry 

Massachusetts Department of 
Agricultural Resources 
Boston, MA 

IDEXX Laboratories, Inc. 

North Grafton, MA 


State Poultry Pathology Laboratories 327 


Diagnostic Cenler for Population and 
Animal Health 

Michigan State University 
Lansing, Ml 

Veterinary Diagnostic Laboratory 

University of Minnesota 
St. Paul, MN 


Diagnostic Laboratory System 

Mississippi Slate University 
Mississippi Slate and Pearl, MS 



Animal Health Diagnostic Laboratories 

Missouri Department of Agriculture 
Jefferson City and Springfield, MO 

Research Animal Diagnostic Laboratory 

University of Missouri 
Columbia, MO 


Montana Veterinary Diagnostic 

Montana Department of Livestock 

Bozeman, MT 



Nebraska Veterinary Diagnostic 

University of Nebraska 
Lincoln, NE 


Animal Disease and Food Safety 

Nevada Department of Agriculture 
Elko and Reno, NV 


New Hampshire Veterinary Diagnostic 

University of New Hampshire 
Durham, NH 


Animal Diagnostic Laboratory 

New lersey Department of Agriculture 

Trenton. NJ 




Veterinary Diagnostic Services 

New Mexico Department of Agriculture 

Albuquerque, NM 



Department of Microbiology and 

Cornell University 
Ithaca, NY 

328 The Chicken Health Handbook 

Duck Research Laboratory 

Cornell University 
Eastport, NY 


Veterinary Diagnostic Laboratory 

North Carolina Department of Agriculture 

& Consumer Services 

Ardcn, Elkin, Monroe, and Raleigh, NC 



North Dakota Veterinary Diagnostic 

North Dakota State University 
Fargo, ND 


Animal Disease Diagnostic Laboratory 

Ohio Department of Agriculture 
Reynoldsburg, OH 


Oklahoma Animal Disease Diagnostic 

Oklahoma State University 
Stillwater, OK 

Animal Health Lab 

Oregon Department of Agriculture 

Salem, OH 


Veterinary Diagnostic Laboratory 

Oregon State University 
Corvallis, OR 

li 1 1 p://oregonstate.eilu/vel med/diagnostic 


Animal Diagnostic Laboratory 

Penn State 
University Park, PA 

New Bolton Center 

University of Pennsylvania 
Kennett Square. PA 

Pennsylvania Animal Diagnostic 

Pennsylvania Department of Agriculture 

Harrisburg, PA 


A member of PADLS 


Department of Agriculture 

San Juan, PR 

Department of Fisheries, Animal, and 
Vetermary Science 

University of Rhode Island 
Kingston, Rl 


Veterinary Diagnostic Center 

Clemson University 



Animal Disease Research and Diagnostic 

South Dakota State University 
Brookings, SD 

State Poultry Pathology Laboratories 329 


C. E. Kord Animal Disease Diagnostic 

Tennessee Department of Agriculture 

Nashville, TN 



Department of Veterinary Pathobiology 

Texas A&M University 
College Station, TX 

/; ttpJIvetmed. tain u, edu/vtpb 

Texas Veterinary Medical Diagnostic 

Texas A&M System 

Amarillo, Center, College Station, and 

Gonzales, TX 


Poultry specific laboratories in Center and 

Gonzales, TX 


Analytical/Chemistry Laboratory 

Utah Department of Agriculture and Food 
Salt Lake City, UT 

801- 538-7128 

Utah Veterinary Diagnostic Lab 

Utah State University 
Logan and Nephi. UT 


Animal Agriculture Laboratories 

Vermont Division of Agricultural Resource 
Management and Environmental 
Waterbury, VT 

802- 244-4510 

www.veniiontagriciu ' 


Office of Laboratory Services 
Department of Agriculture and Consumer 

Harrisonburg, Ivor, Lynchburg, 
Warrenton, and Wytheville, VA 

www. vdacs. 

Veterinary Teaching Hospital 

Virginia Tech 


Washington Animal Disease Diagnostic 

Washington State University 
Pullman and Puvallup, WA 

www. vetmed. ami. ed uldepts_ waddl 
The Avian Health and Food Safety 
Laboratory is located within the Puyallup 


Meat & Poultry Inspection Division 

West Virginia Department of Agriculture 
Charleston, WV 


Wisconsin Veterinary Diagnostic 

University of Wisconsin 
Barron and Madison, WI 


Wyoming State Veterinary Laboratory 

University of Wyoming 
Laramie, WY 

330 The Chicken Health Handbook 


Livestock Pathology Consultation 

Agriculture and Rural Development 

Airdrie, AB 



Animal Health Center 

Ministry of Agriculture 
Abbotsford, BC 


Veterinary Diagnosis Services 

University of Manitoba 
Winnipeg, MB 


Veterinary Laboratory and Pathology 

Department of Agriculture, Aquaculture 

and Fisheries 

Fredericton, NB 



Laboratory Services 

Nova Scotia Agricultural College 

Truro, NS 


Animal Health Laboratory 

University of Guelph 
Guelph and Kemptville, ON 


Atlantic Veterinary College 

University of Prince Edward Island 
Charlottetown, PE 


Department of Pathology and 

University of Montreal 
Saint-Hyacinthe, QC 


Department of Veterinary Pathology 

University of Saskatchewan 
Saskatoon, SK 

Recommended Reading 

Some of the following publications are regularly updated as new information and 
treatments are made available. When requesting a copy, ask for the latest edition. 

Avian Disease Manual, The American Association of Avian Pathologists, 706-542- 
5645,; easy-to-read handbook designed for avian pathology 

Chicken Diseases, F. P. Jeffrey, American Bantam Association, 973-383-8633.;boo\det geared toward the backyard enthusiast. 

Cade of Federal Regulations Title 9 (vaccines), Title 21 (drugs), Title 40 (pesticides), 
United States Government Printing Office, 866-512-1800,; 
U.S. government regulations, including drug use in poultry (available at many 

Poultry Diseases and Meat Hygiene: A Color Atlas, Drago I lerenda and Don Franco, 
Blackwell Publishing, 800-862-6657,; color 
photos illustrating internal organs with various disease conditions. 

Diseases of Poultry, Blackwell Publishing, 800-862-6657, www.blackwellpublishing. 
com; comprehensive tome written in fairly technical language. 

The Federal Register, United States Government Printing Office, 866-512-1800. government regulations, including drug use in poultry 
(available at many libraries). 

Feed Additives Compendium, Miller Publishing Company, 800-441-1410, www.; monthly report on current regulations governing livestock feeds 
(available at agricultural libraries). 

Feedstuffs Reference Issue & Buyers Guide, The Miller Publishing Company, 
800-44 1- 14 10,; annual feed industry report on livestock 
nutrition and disease. 

Poultty Disease Manual, Michael Davis, Texas Cooperative Extension, 888-900- 
2577,; handbook for small-flock owners. 

National Poultry Improvement Plan, htlp://www.aphis.usda,gov/vs/npip; online 
searchable database of flock owners, dealers, and hatcheries of all fowl by state. 

Nutrient Requirements of Poultty, National Research Council, National Academy 
Press, 888-624-8373,; technical discussions and 
feed charts for formulating rations. 



Poultry Health Handbook, L. Dwight Schwartz, College of Agricultural Sciences 
Publications, 814-865-6713,; guide to identifying and 
preventing diseases of chickens and other fowl. 

Veterinary Clinical Parasitology, Anne Zajac and Gar}' Conboy, Blackwell 

Publishing, 800-862-6657,; laboratory manual 
describing how to conduct a fecal examination, with photos of some of the 
parasites dial infect fowl 


(Illustrations are indicated by page numbers in italics; 
charts and tables are indicated by pages numbers in bold.) 

A-avitaminosis. See Roup (nutritional) 
Acantliocephalans, 77, 79, 38 
Acariasis. See Mites 
Acomalacarus gatli, 68, 72 
Acute death syndrome. Sec- Sudden death 

Acute heart failure. See Sudden dcatii syndrome 
Adenovirus. 12(1. 120, 121-122 
AE. Sw Epidemic tremor 
Aedts spp, 63 

Aerosol vaccination, 203-204. 204 

Aflatoxicosis. 140. 141, 156, 164, 218, 245, 275, 291 

and human health, 232,245 
Aggression, 25 
Al. See Influenza 
Airborne infections, 7 
Airsacculitis. 179. See also Mr-sac disease 
Air-sac disease. 8, 110, 113-1 14, 131, 158, 215,246, 

175, 176 

Air-sac mites, 68, 7 1. 309 
Air sacs, 48. 48-49, 54. 179 
Algae poisoning. 39, 155, 163, 176, 246-247 
All-in all-out management, 9, 109 
Mphaiobius iliapermts. See Darkling beetle 
Ambtyommaspp, 68, 74, 74 
Aminoglycosides. 189-190 
Ammonia blindness. SeeConiunctivitis 
Ammonia fumes, 15, 16.112.264 
Amaebotaenia amenta. 90 
Anaphylactic shock. 164, 190 
Anemia, 55. See also Infectious anemia 
Anthelmintics, 80-82. 186 
Antibacterial drugs. See Antibiotics 
Antibiotic residues, 191-192 
Antibiotics, 1 16. 184-185, 186-190, 191 

and fungal infections. 129, 187 

and human health, 191-192,237 

reactions to. 190. 194 
Antihodies.44,45, 197. 198, 199, 199,200-201 
Anlifreeze poisoning, 141, 153, 155 
Anti-fungal drugs. 186, 187 
Antigens, 45, 103, 199, 20C 
Anti-infection vitamin, 28 
Antimicrobial. SeeAntibictics 
Anti protozoal drugs. 186 
Antiseptic, 2 1 
Antitoxin, 1B6. 197, 198 
Antiviral drugs. 186-187 
Aplastic anemia. See Infectious anemia 
-4rgo.5spp.68, 73, 73 
Argostemma githago. 142 

Arizonosis, 8, 1 10, 1 15, 152. 215, 247-248, 294, 295 
and human health, 24fi 

symptoms of, 152, 154, 163, 174, 175, 176,247 
Arrow Universal Warning Symbol, 191, 19) 
Arthritis, 121, 179. 281. Seealso 

Staphylococcic arthritis, Viral arthritis 
Ascaridia galli. See Roundworms 
Ascaridiasis. See lloundworms 
Ascites. See Broiler ascites 
Asclepias spp, 142 

Aspergillosis. 129, 130, 130,248-249 

and human health, 231, 231-232, 248, 249 
resemblance lo: chlamydiosis. 257: 

dactylariosis. 265 
symptoms of, 158, 159. 161, 162, 176,218. 248, 


.Aspergillus flavus. 232. See rt/so Aflatoxicosis 
A. fttmigatus. See Aspergillosis 
■4spergu7i<s infection. See Aspergillosis 
A. ochraceous. SeeOchratoxicosis 
A. parasiticus. See Aflatoxicosis 
Aspergillus poisoning. See Aflatoxicosis 
Attenuation, 201-202 
Autolnfection, 105 

Bacillarv white diarrhea. See Puliorum 
Bacilli, 109. 109 
Bacitracin. 190 
Bacteria. 15. /09, 1 15, 199 

beneficial, 33. 107. 107 

food-borne, 237-243, 238, 240 

opportunistic, 6. 107. 107, 116, 118 

pathogenic, 107, 107, 108 
Bacterial diseases. 59, 62, 108-109, 110 
Bactericide. 2 1,188, 189.190 
llacterin, 200, 202 
Bacieriostat,21, 188, 189, 190 
Beak dip vaccination, 204 
Beak disorders, 34, 228 
Bedbug, 59. 59-60 
Beetles, 59. 60, 60, 86, 90. 90 
Behavior patterns, 23-25 
Big liver disease. See l ymphoid leukosis 
Biosecurity, 9, 195 

Biotin deficiency, 35, 217, 228, 297. Seenlso 

Vitamin B 
Birnavirus, 120, 120 

Blackhead. 8, 39, 84-85, 97, 105, 198, 250 
resemblance to: campylobacteriosis. 256; 
coccidiosis, 261; lymphoid leukosis, 285; 
Marek's disease. 287; Newcastle disease, 
291;tuberculosis, 309; ulcerative enteritis, 312 
symptoms of. 152, 159, 163, 174, 176, 250 
Blindness, 150. See nfjo Conjunctivitis 
Blister burn. 288 


334 The Chicken Health Handbook 

Blood clotting. See Vitamin K 

BlOUd disorders, 56. 106, 179. Sec also Septicemia 

Blood sampling, 149, 149 

Blood type. 55 

Bloom. 247 

Blowout. See Prolapsed oviduct 
Bluecomh, 8, 39. 123. 131. 251 

postmortem results. 174, 175, 176, 251 
resemblance to: campylobacteriosis. 256; 

cholera, 259 
symptoms of, 153, 159, 160, 161, 162, 163. 164, 

Blue green algae, 247. See also Algae poisoning 
Bluestoiie, 187 

Body temperature, 43, 57, 150, 162 
Bones, 34, 48-49, 50-51, 50. 56, 174, 228 
Booster shots, 199,206 
llnrrelia anserina. .see Spirochetosis 
Botulism. 39, 11(1, 155, 163, 164, 174, 1 1 1-1 12. 251- 

and human health. 231, 240, 243, 252 

resemblance to algae poisoning. 246; Marek's 
disease, 287; tick paralysis, 73 
Brain disorders, 34, 179 
Breast blister. 14.51, 117, 189, 252-253, 253 

and human health. 243. 253 
Broiler ascites, 131, 163, 164, 175, 176,253 
Broiler muring syndrome. See Infectious stunting 

Bronchitis. Sea Infectious bronchitis 
Brooder disorders, 135, 138, 2/6, 223-227, 228, 229 
Brooder pneumonia. See Aspergillosis 
Brooding instinct, 24-25 
Buffet germ, 241 
Bugs, 59, 59-60. 72. 73 
Built-up litter system, 1 5, 30-31 
Bumblufoot, 14, 110, 117. 155. 162, 188.189.254- 
255. 255 

and human health, 243, 254 
Bursa of Fabricius. S'eeCloacal bursa 
Bursitis, 51. See also Breast blister 

Cage confinement. 13, 15 

and disease, 103, 105 

and nutrition. 28.31 

and worms. 81. 83, 89 
Cage fatigue, 33, 155, 157, 174, 255, 293. 300 
Cage osteoporosis. See Cage fatigue 
Cage paralysis. See Cage fatigue 
Calcium. 29. 31. 34-35, 193, 189, 228 
Campylobacter fetus jejuni, 238, 238, 240. See also 

Campylobacteriosis, 8, 109, 1 10, 1 1 1, 255-256, 271 

and human health, 109, 231 . 238, 238, 240, 24 1 , 

symptoms or, 152. 156, 164. 175, 176. 255 
Cancer. See Tumors 
Candida albicans. See Thrush 
Candidiasis. 231. 232. See also Thrush 
Canker, 8, 97, 106,256-257 

resemblance to: NewcasUe disease, 291; wet 
pox, 297; thrush, 308 

symptoms of, 158, 160. 161, 162, 174,256 
Cannibalism, 24, 32, 113. 126, 135-138, 194 
Capillaria spp. 84. 86-87 
Capillariasis. .See Capillary worms 
Capillary worms, 84, 80. 86-87, 256, 308 
Caponizing, 195. See also Emphysema 
Carbohydrates, 32, 35 
Carbolic acid. 19 

Carbon monoxide poisoning, 141, 163 
Carcass disposal, 180 
Cardiovascular disorders, 56 
Carriers, 7-8, 8, 182 
Cassia obuisefoliaAM) 
Castor-bean poisoning, 142, 251 
Cats, 106, 145 

Cauliflower gut. .SeeNecrotic enteritis 
Ceca,47, 174 

Cecal droppings. 47. 151,153 

Cecal worms, 84-85, 86-87. 105 


C.niger. 60-61 

Cestodes. .See Tapeworms 

Cestodiasis. .See Tapeworms 

Cheilospirura hanmlosa, 86-87 

Chicken anemia agent. .See Infectious anemia 

Chicken Little syndrome, 24 


brooding of. 223-224 

disorders of, 224-275, 228, 229 

identification of, 221-223 

poisoning in, 141, 143 

vitamin supplement for. 28. 225 
Chiggers. 68, 72. 72. 72 
Chlamydia psinaci. SeeChlamydiosis 
Chlamydiosis, 59, 66, 8. 18. 1 10. 1 14. 257 

and human health, 168, 189, 190, 196, 231, 235- 
236, 257 

resemblance to: erysipelas. 270; influenza, 282 

symptoms of, 153, 158, 176, 177,257 
Clioanataenia infundibular/!, 90 
Cholera, 8, 18,39, 110, 117. 190, 191, 204, 205 

acute, 117, 153, 158, 159, 161. 162. 163, 258-259. 
282, 291,305 

chronic, 117. 154, 156. 158, 159, 161, 162,259. 
259-260, 302 

and human health, 1 17, 259 

resemblance to: campylobacteriosis. 256; 
chlamydiosis. 257; chronic respiratory 
disease, 259; colibacillosis, 263; erysipelas, 
270: infectious coryza, 279; spirochetosis, 304 

symptoms of. 162, 164, 174, 175, 176 

and ticks. 59, 73 
Chloride. 193, 228 

Chlorine-based disinfectants, 19. 20, 209 
Choking, 164 

Chondrodystrophy. See Slipped tendon 
Chronic respiratory disease. 8. 110. 113-114. 196, 
205, 207.214 215. 260 

Index 335 

resemblance to: air-sac disease. 24(i; infections 
coryza, 279; influenza, 282 

symptoms of, 152, 156. 159, 161, 175, 176, 260 
O'me.vspp. 59,59-60 
Circling disease. See Listeriosis 
Circulatory system, 55. 57. 175 
Claviceps purpurea. See Ergotism 
Claw disorders, 34 

Cloaca! bursa, 45, 45. 45, 4R. 174. See also 

Cryptosporidiosis. Infectious bursal disease 
Cloacitis. .Si;.' Pasted vent 
Closed flock, 10-11 

Clostridial riei matomyositis. See Necrotic 

Clostridial diseases, 110, 111-112, 1811 
Clostridium holuliuum. 238, 240. See also Uolulism 
C colinum. See Ulcerative enteritis 
C perfringens, 238, 240. See also Necrotic enteritis 
Clostridium poisoning, 1 1 1-1 12, 231, See also 

C. septicum. See Necrotic dermatitis 
Clubbed down, 216. 217 
Cocci, 109, 109 
Coccidiasis, 98 

Coccidiosis, 18. 18, 97. 98-9, 102-104, 205, 188. 225 
cecal, 102. 152. 163, 250, 261 
intestinal, 152, 156, 160, 163.261-262,289. 275. 

and nutrition, 28, 32, 33, 228 
symptoms of, 100-101, 102. 174, 175 

See also Cryptosporidiosis 
Coccidiostats, 29,52. 103, 103-104, 143 
Cock-feathered hens, 54 
Coffee seed poisoning, 140. 153 
Colds. See Infectious coryza. Infectious bronchitis, 

Respiratory disorders 
Colibacillosis, 29,35, 110, 112,215,218, 262-263 

and human health, 1 15, 231, 23B. 240 

postmortem findings, 175, 176, 177,262 
resemblance to: chlamydiosis. 257; cholera, 258; 
erysipelas. 270 

symptoms of, 153, 157, 161. 164,262 

treatment of. 188. 189. 190, 191 
Coliform, 112 
Colitis, 231,240.243 
Collyriiium falia. 92 
Comb. 148 

color. 159-160 

and fertility, 214, 218 

frostbitten. 132-133 

removal, 133-134 

See also Favus 
Competitive exclusion, 107, 193-194 
Compost, 15.21, 180 
Confinement housing, 13, 15 
Congenital loco. See Congenital tremor 
Congenital tremor, 154, 220, 263, 268-269 
Conjunctivitis, 16, 161, 179, 263-264 

and human health. 231, 236 
Constitutional vigor, 1 1.217 

Contagious catarrh. .See Infectious coryza 

Copper deficiency. 32. 35, 228 

Copper sulfate. 187 

Corncockle. 142 

Coronavirus, 120, 120 

Coryza. See Infectious coryza 

Crazy chick disease. See Fncephalomalacia. 

Congenital tremor 
CRD. See Chronic respiratory disease 
Creeper gene, 220 
Cresol, 19.20 
Cresylic acid, 19 

Crop binding. Set-Crop impaction 

Crop disorders. 160, 174 

Crop impaction, 46. 131. 160, 264, 174, 195 

Crop mycosis. See Thrush 

Cropping, 1 16, 133-134. 195 

Crop worms. 84, 86-87 

Crotalaria poisoning. 140, 153 

Crowing, 24 

Crud. See Necrotic enteritis 
Cryptococcocus neofornums. 231, 232 
Cryptococcosis, 231 , 232 

Cryptosporidiosis. 97, 101-105, 154, 158, 159, 163, 

265, 291,312 
Cryptosporidium liaileyi. See Cryptosporidiosis 
Cuclologaster helemgraphus, 64, 64, 65, 66 
Ctilex spp, 63 
Culicoides spp. 62 
Culling. 11-12. 181-182.220 
( .tirlcd-loc paralysis. 3 1 , 33, 227. 268 
Cyanobacleria, 247 
Cylodites iiudus, 68,71 

Oaetylaria gallopaua. See Dactylariosis 

Dactylariosis, 129. 130. 130, 154,248.265-266 

Darkling beetle, 59, 60. 60, 90 

Daubeutonia luitgifolia, 142 

Davainea proglottina. 89. 90 

Dead birds, disposal of, 180 


of chicks, 223. 225. 226 

diseases causing, 79, 1 63-164 

of embryos. 211,216. 217, 218-219 

rate of. 1 65, 1 67 

See also Septicemia 
Deathcamas, 142 

Debeaking, 64, I IB, 138-139, 139. 195 
Decrovving, 195 

Dehydration. 40-41,41, 48, 54, 156, 180, 193, 226 
Dermauyssus gallinae, 67, 67, 68 
Dermatitis, 288. See also lirgolism, Necrotic 

Dermogylplms spp, 68 
Detergent, 17, 19,21,209 
Diagnosis, 147, 148. 150, 165. 195,244 
Diarrhea. 151,152-153 

and antibiotics, 190 

and dehydration. II, 193 

and drug absorption. 183 

336 Tub Chicken Handbook 

Diarrhen (conlimieit) 

and enteritis, 47, 123.150 

andriotritlon, 31.227 

and stress, 23 

treatment of, Iflti 

and worms. 79 
Digestive disorders, 56, 7? 

Digestive system. 46-48, Jfj. 172. 172. I'X llltl 
Dikkop. See Swollen head syndrome 
Diphtheria. See Infectious laryngotracheilis. Pox 

Direct contact, ti, /> 
Disease. 3 
Disease cycle, 2 1 1 
Disease history, 166 
Disinfectants. 19-21.20, 1411.21 1-213 
Disinfection, 17-18 
Disphurynx nfisulo, 86-87 
Displacement activity. 25 
Distemper. See Newcastle disease 
Donald Duck syndrome 220 
Drenching. 183, 183-184 
Droppings. 148, 228 

cecal, 47, 151. 153 

and flies, 62-63 

and disease, 34, 151. 152-153 

and parasites, 93 

See also Diarrhea 
Droppings boards, 14 
Dropsy. See Broiler ascites 
Drugs, 13, 181. 182. 183-186. 195 

antibiotic, 186-190 

anticoccidial, 103, 103-104 

dilution of, 184 

and nutrition, 33 

and stress, 22 

and water consumption, 23, 40 

worming, 80-82 
Dubbing, 113, 116, 126, 133-143. 195 
Dust baths, 24, 75-76 

Echidimphaga galliiwcert, 6 1 
Ectoparasite. See Parasite (external) 
Egg binding, 33 

Egg drop syndrome, 120, 121-122, 131, 156,157, 

215, 266. 276 
Egg eating, 23. 29. 137 

double-yolked, 51 

and disease, 1 14-1 15.215, 215, 2/8 

disorders of, 29, 34-35, 52, 53, 156-157 

evaporation from. 209. 210 

fertility of, 213-214 

fomiarion of, 51-52, 52 

hatchability of, 215-217 

hatching, 208-211, 213,218-219 

and human health. 237-24 1 , 242 
Eimeria spp. See Coccidiosis 
Electrolytes, 193, 193 
Embryo death, 21 1, 216. 217. 218-219 

Embryo dyeing, 221-222,222 
Einbryonation. 7A.83 
Emphysema, 267 
Encephalitis, 179,269 

I ricephalornalacia. 33, 154, 156,161.267,267-268. 

263, 265, 269, 284 
Encephalomyelitis. See Epidemic tremor 
Endoparasites. See Parasites (external) 
Energy, 32 

Enlarged hock disease. Seelnfectiocs synovitis 

En teric diseases. See Enteritis 

Enteric Newcastle disease, 125 

Enteritis. 39, 47. 57, 123, 150, 152-153, 179,189. 
192, 262. See also Bluecomb, Colibacillosis, 
Infectious stunting syndrome. Necrotic 
enteritis. Rolaviral enteritis. Ulcerative 

Enlerohepatitis. See Blackhead 

Enierotoxemia. S'eeNecrotic enteritis 

Epidemic tremor, 59, 73. 120. 123, 131, 201, 205, 
215, 268-269,269 
resemblance to: congenital tremor, 263; 

listeriosis, 284; Marek's disease, 287 
symptoms of, 154, 156, 161, 163,268 

Epiclermoples bilobatiis. 68, 70 

Epson salts, 192 

ErgOUSm, 140, 141, 153, 154, 160, 175, 269 
ErySipelaS, 8, 18, 1 10, 113, 204, 205,258, 269-270 
and human health, 1 13, 231, 236. 270 
postmortem findings, 174. 175, 176, 177,270 
symptoms of, 152, 156, 158, 163,164, 270 

Erysipeloid, 231, 236 

Brystpelothrix rhusiopnihiae. See Erysipelas 
Erythroid leukosis, 128 
Erythromycin, 190 

Escherichia coli, 238, 238, 240. See a!so Colitis. 

Ethology, 23 
Ethylene-glycol, 141 
European fowl pest. See Influenza 
Excretory system, 48 
Exhibition. See Showing 
Exudative diathesis, 33, 159. 270-271 
Eye disorders, 28, 35. 105, 161, 179, 228 
Eye vaccination. 2114. 205 
Eye worms. 85,86-87,88, 161 

Facial Cellulitis. See Swollen head syndrome 

False botulism. SeeMarek's disease 

False layer, 53 

Fans, 16, 135 

Farmer's lung, 231, 233 

I 'alal syncope. See Sudden death syndrome 

PaBJf liver syndrome. 33, 131. 245. 271-272 

postmortem Findings, 175. 176, 271 

symptoms of, 153, 154, 156, 159,164,271 
Favus. 129. 130, 130,159,160,272 

and human health, 272 
Feathers, 148 

discoloration of. 159, 228, 229 

Index 337 

disorders of, 27, 35, 140 

and lice, 64, 65, 66 

loss of. 137 

and miles, 68, 70-71 

and wounds, 194 
Fecal testing, 82-96, 102 
Feeders. 37, 37, 136 
Feeding schedule, 36 
Feedstuffs. .See Rations 
Fertility, 23, 213-214 
Fever, 43, 57, 150, 162 
Flatworms, 77. 79, 89 
Fleas, 60-61, 61 
Flies, 59, 61-63. 62, 90 

Flip-over disease. -See Sudden death svndrome 

Flock history, 9 147, 148. 166 

Flooring, 14 

Floor space, 14, 15 

Flukes, 77, 79, 69. 90-92, 92, 153 

Flushes, 192 

Fly trap, 63 

Fomiles, 5, 7 

Food poisoning, Set' Botulism 

Formaldehyde, 178, 212 

Fowl pesl. .See Influenza 

Fowl plague. 2S0. .See also Influenza 

Free range, 13, 26 

and disease. 105. 103. 113 

and worms. 79, 81 . 83, 88, 89 
Frizzledness, 221,228 
Frosthite. 132-133 
Fumigation. 212-213 
Fungal diseases, 129, 130, 187 

in humans. 231-232 
Fungal poisoning, 129, 140-141. 141. 153. 245, 269, 
273, 292 

in humans. 232 
Fungicide. 21, 143. 190 
Fungistat,21, 190 

Fusariotoxicosis, 140, 141, 156. 157. 162, 163,272- 

and human health, 273 
Pusatjum spp. See Fusariotoxicosis 

Gangrene, 133. See also Necrotic dernialilis 
Gapes. See Gapewornis 
Gapeworms, 80, 86-87, 88, 280 
Gas edema disease. .See Necrotic dermatitis 
Generalized disorders, 55, 56. See also Septicemia 
Genetic disorders, 156, 214, 218-219, 220-221, 226, 

Genetic resistance. 1 1-13, 198. 207 
Gentamicin, 189 
Germicide, 21 
Gizzard worms, 86-87 

Qottidium vesicarium, 142 
Going light. .Set- anemia 
Gongj'ltmema ingluvicola, 84. 86-87 
Goniocotes gallium; 65, 66 
G'omorfe.vspp, 65,66 

Gossypolseed poisoning, 140. 160 
GOUt 27. 33. 39 

articular. 48, 155,273 

visceral, 131,273-274 
postmortem findings, 174, 175, 176,177,274 
symptoms of, 157, 159, 163, 164,273 
Gray eye. .See Marck's disease 
Greens. See Bluccomb 
Grooming activities. 24 
Gross lesions, 173 

Growth promoters, 184-185, 190.237 
Gumboro disease. .Sec Infectious bursal disease 

Haemamsiphnn moihn a, 59 

Haemophilus paragallinarum. See Infectious 

llatchability, 23, 215-217 
I latching eggs, 208-209 
I lead, swollen. See Swollen head syndrome 
Health signs. 148 

Heart attack. SeeSudden death syndrome 

Heart rate, 43 


as disinfectant, 21 

and egg production, 52 

and nutrition, 32. 33 

stress, 28, 134-135, 136, 140 

and water consumption, 40, 40, 4 1 
Helicopter syndrome. See Infectious stunting 

Helminthiasis. See Worms 
Hemophilus infection. See Infectious coryza 
I lemorrhagic anemia syndrome. See Infectious 

Hemorrhagic septicemia. SeeChoIera 
Hen worker's lung, 231, 232-233 
Hepatitis, 179. Seei/to lllackhead, 

Campylobacteriosis, Infectious anemia 
Hereditary disorders, 156, 214, 218-219. 220-221, 

226. 227 
Herpesvirus. 120. 120 
1 hienikis galliiuirum. See Cecal worms 
Histomonad infection. See Blackhead 
Histomonas meleagriclis. See Blackhead 
Histomoniasis. See Blackhead 
Histopliisniti C(ii>suhtlnni. See I lisloplasmosis 
Histoplasmosis, 129, 130, 130, 153, 176, 177,274- 


and human health, 130, 231 , 233-234. 275 
Host, intermediate, 78, 78-79, 81 
Housing, 13-14, 15, 17 
Human health, 23(1, 231, 244 

and antibiotics, 191-192,237 

and environment, 231-234 

and parasites. 234-235 

and poultry products, 237-242, 238, 240, 242, 


and zoonoses, 235-237 
Humidity, 33, 135 

and incubation. 2111-21 , 218-219,226 

338 The Chicken Health Handbook 

Hydrogen peroxide, 194 
Hymenolepisspp, M 
Hypochlorites, 19 

1BD. See Infectious bursal disease 
Immunity, 197-199. 199 

and allatoxicosis. 140 

and blood type, 55 

boosters, 193-194 

breeding for, 1 1-13 

indicators of, 12, 167 

natural, 12, 198,207,224 

and nutrition, 26. 28, 31 

and stress, 22, 23 

suppressed, 122,206,207 

and viruses. 1 19. 121 

and wormers, HI -82 

to worms, 77, 79, 83. 85 
Immune system, 44-45. -15 
Immunoglobulin. See Antibodies 
Impetigo, 243, 254 
imprinting. 25 

Inbreeding, 217, 218, 220-221 
Incidence, 244 

Inclusion body hepatitis. See Infectious anemia 

Incubation, 210-21 1, 218-219 

Incubation period, 244 

Incubator sanitation. 21 1-213 

Indicators, 12, 167 

Indirect contact, 6. 6 

Infection. 4. 108 

Infectious anemia, 33, 45,55, 120, 121, 131,215. 
200, 245, 275-276 
postmortem findings. 174, 176, 177,275 
resemblance to: campylobacteriosis, 256; 
coccidiosis, 261; infectious stunting 
syndrome, 280; ruining syndrome. 303 

resemblance to; cholera, 259; chronic 
respiratory disease, 2B0; infectious 
bronchitis, 276; swollen head syndrome. 307 
symptoms of, 156, 158, 160, 161,278 
vaccination against, 203 204, 205. 207 
Infectious diseases, 3-4, 4, 107 
Infectious encephalomyelitis. See Epidemic tremor 
Infectious enterohepatitis. See Blackhead 
Infectious hepatitis. See Campylobacteriosis 
Infectious laryilgotracheitis, 8. 11, 18, 120, 124. 
196, 279-280 
resemblance to: aspergillosis, 248, 249; 

infectious bronchitis. 276; infectious coryza. 
279; influenza, 282; Newcastle disease, 291; 
wet pox, 297 
symptoms of, 156. 15"7, 158, 161, 163, 279 
Vaccinal ion against. 20 1 , 205, 206 
Infectious leukemia. Sec Typhoid 
Infectious sinusitis. See Chronic respiratory disease 
Infectious stunting syndrome, 121, 123.131.215. 
symptoms of, 152, 159,280, 175, 177 
Infectious synovitis, 8, 51. 1 10, 1 13-1 1 4. 215, 281, 

postmortem findings, 175, 176,281 
resemblance to; breast blister. 252; paratyphoid, 

294, viral arthritis, 122 
symptoms of, 152, 154, 158, 159, 162, 262. 28J 
vaccination against. 205 

symptoms of. 152, 159, 163, 164, 275 
Infectious bronchitis, 8, 18, 48, 120, 122, 200, 211, 

postmortem findings, 174, 175, 177,276 
resemblance to: Aspr 

respiratory disease, 259; 

266; infectious coryza, 279; infectious 

laryilgotracheitis, 279; influenza, 282; 

Newcastle disease, 290; swollen head 

syndrome, 307 
symptoms of. 156, 157, 158, 161. 163,276 
vaccination against, 201, 203, 205, 207 
Infectious bursal disease. 18. 18, 39, 45. 45, 120. 

122-123. 277-278 
postmortem findings, 174, 175, 177,277 
resemblance to: infectious anemia. 275; runting 

syndrome, 303 
symptoms of, 152, 154, 162, 163,277 
vaccination against, 201. 205, 207 
Infectious catarrh. See Infectious coryza 
Infectious coryza. 8. 18, 39, 1 10, 1 12-113, 214, 278. 


Influenza, 8, 18. 120. 123-124, 196, 200, 282 
and human healdi. 282 
resemblance to: chlamydiosis. 257; egg drop 

syndrome, 266; Infectious coryza, 279; 

Newcastle disease, 291: spirochetosis, 304 
symptoms of, 153, 156. 157, 158, 160, 161, 162, 

Injury. 194 
Insecticides, '. 
Insects, 58. 59 
Interferon, 187 

Intermediate hosts. 78, 78-79, 81 

Internal layer, 53 

Intestinal coccidiosis. 

Intestinal disorders, 56, 77, 175, 179 

See also Enteritis 
Intraocular vaccination, 204 
Iodine deficiency, 217 
Iodine disinfectants. 19, 20. 209 
Iritis. SeeMarek's disease 
Iron deficiency, 228 
Ivermectin. 70. 76, 80. 87 

littery chicks. See Congenital tremor 

Index 339 

ratal disorders. 50-5 1 . 56, 179. See also Infectious 
synovitis, Staphylococcic arthritis 

Keel bursitis. See Breast blister 
Keel cyst. Sec Breast blister 
Keel deformity, 35 

Keratoconjunctivitis. See Conjunctivitis 
Kidney disorders, 179 
Killing chickens, 168, 168-169, 182 
Kinky back. 154.163,283 
Knemidocoptes spp. 68. 69-7 1 

Lameness. 15-1-155, 173. See also Legs 

Lamtntoptes cysticola. 68, 71 

Laryngotracheitis. See Infectious Inryngotracheitis 


color oL 154-155 

disorders of, 35, 50, 228 

and miles. 68, 69-70. 70 

thick. See Osteopetrosis 
Lesions, 173-174, 174-177, 177, 244. See also 

Inflammation. Tumors 
Lesser meal worm. See Darkling beetle 

Lethal genes, 220-221 

Leucocylozoon spp. See Leucocytozoonosis 
Leucocytozoonosis. 8, 39, 59, 61-62, 97, 106, 283- 
284. 286 

postmortem findings, 175, 177, 284 
symptoms of, 152, 154, 158, 162, 163, 283-284 

Leukosis complex, 126, 128,215.309 

Lice, 59, 63-67, 6* 65, 160 

Life span, 43 

Limbenieck. See Botulism 
Lipeunis caponis, 65 
Listeria otonocylogenes, .Sep Listeriosis 
Listeriosis, 8, 1 10, 1 18. 284-285 

and human health, 231, 236-237, 285 

symptoms of, 152, 154, 164, 175, 176,284 
Litter, 14-15,62-63 

and coccidiosis, 99 

eating of, 24, 225 

and scavenger mites, 72-73 

and worms, 89 
Liver disorders. 179 
Long-bone distortion. Sep Twisted leg 
Lymphatic system, 44 

Lymphoid leukosis, 8, 45, 121, 128, 215, 285 
postmortem findings. 174. 175. 176. 177, 285 
resemblance to: fatty liver syndrome, 245; 
campylobacteriosis. 256; Marek's disease, 
128, 128, 287 
symptoms of, 152, 156, 159, 164, 285 

Macrolides, 190 

Magnesium deficiency. 31. 34-35, 193, 217 
Magnesium sulfate, 192 

Malabsorption, 33. Seealso Infectious stunting 

Malaria, 59, 63, 97. 106. 164, 284, 286 
Malignant edema. See Necrotic dermatitis 

Manganese deficiency, 32, 35, 138. 217, 226. 228 
Marble bone. See Osteopetrosis 
Marek's disease, 8, 18.45,45,59, 120,126-128. 127, 
and human health. 127-128. 288 
and natural resistance, 55, [98 
postmortem findings, 175, 176, 177,287 
resemblance to: botulism, 251-252; cage fatigue, 
255; congenital tremor, 263; lymphoid 
leukosis, 128. 285; runting syndrome, 129. 
303; spirochetosis. 304; toxoplasmosis. 309 
symptoms of, 155, 159. 161, 163, 164,286 
vaccination against, 201, 202, 204. 205, 207 
Mechanical vector. 6 
Medications. See Drugs 
hiegnlnia app, 68,71 

Mciiacamhiisspp, 64. 64, 65, 66 

Menopon gallimu, 65, tit; 

Mice, 143, 143-146, 144 

Microflora, beneficial, 47. 108. 129. 187, 190, 193- 

Mycropolyspora faeni, 231, 233 
Miamponun gallinae. See Favus 
Milkweed poisoning, 142 
Minerals, 31-32 

chigger, 68, 72, 72,72 

external. 67-73, 67, 68, 6a, 72 

and human health, 231, 234 

internal, 71-72 

resemblance to lavus. 272 

scavenger, 72-73 

symptoms oL 160, 162 

See also Ticks 
Molasses Hush. 192 

Moldy feed, 36, 37, 129, 140-141, 141. 153, 245, 269, 

273. 292 
Moldy litter, 15 
Moiling, 27,54,137 
Moniliasis. See Thrush 
Monocytosis. See Bluecomb 
Mortality. 244 . See also Death 
Mosquitoes, 59,63, 106 
Mothballs, 139 

Month disorders. 35, 162, 228 
Musca doineslica, 62, 62-63 
Mucous Membrane, 44 
Mud fever. See Bluecomb 
Mugtiet. .See Thrush 

Muscle disorders, 35, 150, 154-155,228 

Muscular dystrophy. See White muscle disease 

Mushy chick disease. SeeOmphalitis 

Mas musculus. 143, 144 

Mycoplasma gallisepticum. See Air-sac disease, 

Chronic respiratory disease 
Mycoplasmas. 109, 189 
Mycoplasma synoviae. See Air-sac disease, 

Infectious synovitis 
Mycoplasmosis. 18, 110, 1 13-114, 189. 190.257 
Mycoses. See Fungal diseases 

340 Thk Chicken Health Handbook 

Mycotic diseases. Seelungal diseases 
Mycotic pneumonia. See Aspergillosis 
Mvculoxicosis. 129, 140-111, 141, 153.245(26$ 

Myeloid leukosis. 128 

National Poultry Improvement Plan, 10. 110 
Navel infection. See Omphalitis 
Necropsy. See Postmortem examination 
Necrotic dermatitis, 110, 111. 154, 159,163, 164. 

and human health, 289 
Necrotic enteritis. 110.261, 152, 163,164. 175,289 

and human health, 231, 240, 241. 243, 289 
Neinathelininthes, 77,79,82 
Nematodes. See Roundworms 
Neomycin, 189-190. 194 
Neoplasm, SeeTumors 
Neoscliungasii a. ainerkaiia. 68, 72 
Nephritis, 179 

Nephrosis. See Gout (visceral), Infectious bursal 

ff$FiiUm uletmcler. 142 
Nervous system, 5 1-55 

Nervous disorders, 55, 56, 57, 150, 154-155, 228 
Neuritis. See Marek's disease 
Neurolyinphomalosis. See Marek's disease 
Newcastle disease. 8. 18, 39, 120, 124-125, 125, 

and human health, 231, 236. 290, 291 
resemblance to: Ariznnosis, 247; Aspergillosis, 

248. 249; cholera. 259; chronic respirator)' 

disease. 259; egg drop syndrome, 266; 

epidemic tremor, 269; erysipelas, 270; 

infectious bronchitis, 276; infectious coryza. 

279; infectious laryngoiracheitis, 279; 

influenza, 282; listeriosis, 284; Marek's 

disease. 287; spirochetosis. 304: swollen head 

syndrome, .107; toxoplasmosis, 309 
symptoms of, 153, 154, 155, 156, 157, 158, 159, 

161, 162, 164, 290. 291 
vaccination against, 201 , 205, 207 
\i w England disease. SeffBpidemtc tremor 
New-house coccidiosis syndrome, 99 
New wheat disease. SeeBluecomb 
Nicotine sulfate, 76, 139 
Nightshade. 142 
Noninfectious diseases, 3 
NPIP, 10,116 

Nutritional disorders. 26-27, 33, 33-34, 34-35, 137, 
178-179, 180. 
in breeder docks. 214, 216. 217 
in chicks, 225, 226. 227. 228, 229 
Nutritional myopathy. See White muscle disease 
Nutritional roup. See Roup (nutritional) 
Nutritional supplements, 27, 28, 31, 193,216. See 
also Rations 

Obesity. 39.214.218 

Ochratoxicosis, 140. 141, 153. 157, 175,176,292 

and human health, 292 
Ocular lymphomatosis, See Marek's disease 
Odor and disease. 160 
Oea'flci/swcarius. 59 
Oidica. See Thrush 
Oidiomycosis. .SVeThrush 
Oleander, 142 

Omphalitis, 39. 1 10, 1 1 1, 1 17, 215, 219, 292-293, 

and human health, 293 

resemblance to pullorum, 299 

symptoms of, 152, 160, 262. 292 
Oocysts. y& 98-99, 101,104 
Open housing, 15 

Opportunistic infections, 6. 107, 107, 116, 1 18, 121 

Oral drugs, 183-185 

Organic production, 237. See ulsu l-'rce range 
Organs, internal, 46, 49, 52. 1S9, 170 

membrane surrounding, 179 

tissue samples of, 1 78 

Uriiiilumyssus spp. 68, 69. 69 

Ornithosis. See Chlamydiosis 
Orthomixovirus, 120, 120 
Osteomalacia. See Rickets 

Osteopetrosis, 121. 128, 155, 162, 174, 215, 293- 

Osteoporosis. See Cage fatigue 
Ovaries, 51. 52, 54, 126 
Oviduct disorders, 179 
Oviduct flukes. 91, 92, 153 
(Jxysplnm nmnsoni, 85, 86-87, 88 

Pale bird syndrome. See Infectious stunting 

Panting, 134-135 

Paracolon. SeeArizonosis 

Parainfluenza. See Newcastle disease 

Paralysis, 154, 173. 227 

Paramyxovirus, 120. 120,290, 291 

Parasites, 4, 58, 136,214 
external. 58, 59, 74-76 
and human health, 231, 234-235 
internal, 8, 77, 79-82, 97-98, 106 
and nutrition, 29, 3 1 . 33. 35, 79. 228 
See also Bugs, Pleas, Flies, Lice, Mites, Ticks, 

Paratyphoid, 8, 1 10, 1 15, 215, 219. 294-295 

and human health, 1 96, 23 1 , 239-24 1 , 24 1 . 295 
postmortem findings, 175, 176, 295 
resemblance to; paratyphoid, 247; pullorum, 

299; typhoid, 311 
symptoms of, 152, 156, 159, 161, 162, 163, 294 

Parrot fever. See Chlamydiosis 

Parvovirus. 275 

Pasted vent, 152, 160, 295-296 

I'asieurella nmltocida. See Cholera 

P. septka, 259 

Pasteurcllosis, 110, 117, 190, 257 
Pathogenicity, 22, 107 

Index 341 

Pathogens* 18, kit. 107, 150 

Pathologist. 165. 167 

Pathology laboratory, 165-167, 168, 178 

Peck order, 25,203.214 

Pediculosis. See Lice 

Pedigree. 12 

Pedigree baskets, 223 

Pendulous crop. See Crop impaction 

Penicillin. 188-189. 191, 192 

Penicillium pubenilum. SeeAflatoxicosis 

P. viridkauim. SeeOchratoxicosis 

Pericarditis, 179 

Peristaltic action, 53 

Perosis. .See Slipped tendon 

Pesticides, 75-76, 80, 143, 164, 237, 269 

Phenol. 19, 20 

Phllophthalmus grain. 92 

Phosphorus, 31. 34, 193, 228 

Physiological zero, 209 

Phytolacca americana, 1 42 

Pickout. Sec Prolapsed oviduct 

Picornavirus, 120. 120 

Pink disease. .See Fatty liver syndrome 

Plague. .See Newcastle disease 

Plantar pododermalitis. See Bumblefnni 

I'lani toxins, 142 

Plasmodium spp. .See Malaria 

Plalyhelminihes, 77. 79, 89 

Pleuropneumonialike organism infection. See 

Chronic respiratory disease 
Plumage. See Feathers 
Pneumatic bones. -18—19. 50 
Pncumoencephalitis. See Newcastle disease 
Pneumomycosis. See Aspergillosis 
Pododermatiiis, SeeBumblcfool 
Poisoning, 139, 258. 275 

algae. 39, 155, 163, 246-247 

antifreeze, 141, 153, 155 

bacitracin, 190 

in chickens, 108. 111-112 
in humans. 231. 237-238. 238, 239-242, 240, 

coccidiostat. 143 
copper sulfate. 187 
fungal, 129, 140-141. 141 
naphthalene, 139 
nitrofurazone, 143 
pesticide, 143, 164.269 
plant. 142 

rodent, 145-146, 146 

rose chafer, H3 

seed, 140 
selenium, 32 
sulfamethazine. 103 
treatment of, 192 
Pokeberry poisoning, 142 

Postmortem examination, 165, 769, 170, 171, 171- 
documentation of, 177-178 

do-it-yourself, 167-168 

interpretation of 173-174, 174-177, 177 

professional, 165-167 

specimen preparation for, IBS, 168-171, I'l 
Potassium. 32. 34-35, 193 
Potassium permanganate, 212 
Potato poisoning. 142 
Poultry meal, 237-238, 24 1 , 242, 243 
Pox, 8. 18, 59, 63. 120, 162, 126, 237 

dry, 156, 160, 296-297 

wet. 28-29. 164, 256, 279. 297-298, 308 

vaccination against. 201 , 202, 205, 206 
Poxvirus, 120, 120 

PPl.O. See Chronic respiratory disease 

Preconditioning, 22, 23 

Progeny testing, 12 

Prolapsed oviduct, 33, 52. 53 

Prosllwgoiiimus spp, 92 

Protein. 27-28, 32, 34-35, 228 

Protozoa, 15, 97-98 

Proiozoan diseases, 97 

Pseudo-botulism. .See Marek's disease 

Pseudofowl pest. See Newcastle disease 

Pseudomonas, 110, 118. 188. 191.215, 218, 298 

and human health. 231. 234, 298 

symptoms of, 153, 155, 164, 175, 176, 177, 298 
Pseudomonas aeruginosa. See Pseudomonas 
Pseudo-parasites, 93 

Pseudo poultry plague. SeeNewcasUe disease 
Psittacosis. SeeChlamydiosis 
Plerolichtts ohsiuses. 68 
Pullet disease. See Bluecomh 
Pullorum. 8, 1 10, 1 15. 196, 215, 298-299 
and human health, 299 

postmortem findings, 174, 175, 176, 177,299 
resemblance to: campylobaeteriosis, 256; 

lymphoid leukosis. 285; paratyphoid, 294; 

typhoid. 311 
symptoms of. 152, 153, 158, 159, 163, 164, 298- 


Pycnoscelus surinumensis, 85. 88 
Pyrelhrum, 75 
Pyridoxine deficiency, 268 

Quail disease. See Ulcerative enteritis 
Quaternary ammonium compounds, 19,20,209 
Quicklime, 19 

Rachitic chicks. See Rickets 

Range-fed chickens. .See Free range 
Range paralysis. See Marek's disease 
Rations. 25, 31. 36-37 

and antibiotic resistance. 184, 191 

and cannibalism, 136, 138 

consumption of. 37-38. 38, 135, 148, 192 

digestion of, 46-48 

drugs in. 184-185 

and fungal toxins. 140-141. 141 



Rations (continued) 

and pesticides, 237 

-related disorders. 39. 226. 227 

and toxic seeds. 140 
Rats. 143, 143-144, 144. 144-146 
llatlusspp, 143, 144 
Recessive genes, 220-221 
Reflex behavior, 23 
Renal failure, SVeGout (visceral) 
Renal gout. SeeGout (visceral) 
Reovirtis, 83, 121. 121 
Reportable diseases. 196. 196 
Reproduction, 23, 29, 30, 55, 213-214 
Reproductive system, 51-54, 52, 56, 156-157 
Reservoirs of infection. 4-5. 224 
Resistance. See Immunity 
Resistance factor, 55 
Respiration rate, 15-16, 43 
Respiratory disorders. 16, 49-50, 56, 77.176, 186 

and cryptosporidiosis, 105 

and Marek's disease, 287 

and salpingitis. 53-54 

symptoms of, 57, 150, 158 

and vitamins. 28-29. 35 

See also Air-sac mites 
Respiratory system, 48-19, 49, 172-173 
Restricted feeding, 38 

Reticuloendotheliosis. See Ruining syndrome 
Retrovirus, 121, 121 
Rhinitis. 179 
Rib disorders, 35 

Riboflavin deficiency, 180, 216, 217. 227. 228. 269. 

RlBilTUS communis. 142 

Rickets, 33, 154, 155, 159, 174, 228, 300. 255, 269, 

293, 300-301 
llivollasin bifurctiln. 68, 7 1 
Rodent bait station, 145 
Rodenticides. 145-146, 146 
Rodents. 13, 14, 143-146. 144, 143 
Roosts, 14 

Rotaviral enteritis. 121, 123. 152, 163, 174, 175, 

Rotavirus, 121, 121 
Hot gut. See Necrotic enteritis 
Round heart disease, 131, 164, 175,301-302,307 
RmtndWdnni, 14, 77. 78, 78-79, 79, 80, 82-88, 86- 

87, 773,228,261 
Roup, 49 

nutritional. 28, 33, 158, 16 1 , 1 61 , 276, 279. 29 1 , 
Humplcssness, 221 

Hunting syndrome, 45, 121, 129, 131, 154, 174.215, 

280, 302-303 
Ruptured tendon. See Viral arthritis 
Rye seed poisoning, 140, 153. 155 

Salmonella arizonae. SeeArizonosis 
S. enlerilidis, 238. Sec also Paratyphoid 
S. gallinarium. See Typhoid 

S. Heidelberg, See Paratyphoid 
S. pullorUm. Sec Pullorum 

Salmonella spp. 238. 240. See also Salmonellosis 
S. lypUitniirium. See Paratyphoid 
Salmonellosis. 18,39, 110. 1 14-116. 174, 175, 215, 

and human health, 231. 238, 239-241 , 240 

resemblance to: blackhead. 250: coccidiosis, 
261; erysipelas, 270 

and selenium, 32. 35 

treatment of. 189. 190. 191 
Salpingitis. 53-54, 179, 262 
Salt, 31-32. 35, 138 

deficiency, 156 

poisoning, 32. 39, 253. 269 
Sanitation, 17,21,211-213. 238 
Sanitizers, 20, 21, 209, 238-239 
Scaly-leg mites, 68, 69-70, 70. 155 
Scatology, 151, 152-153 
Scoliosis, 221 

Secondary infection, 188. 193 
Selenium, 32. 35, 180, 217, 228 
Self-limiting infections. 182 

Septicemia. 55, 57, 108, 117, 179, 189, 251. 262. See 

also Generalized disorders 
Sex change, 54 
Sexual behavior, 24, 54 
Shock. 164, 190. 194 

electrical, 226 
Shols, 183-184, 185-186 

and debeaking, 138 

and disease, II, 182 

and dubbing, 134 

and stress, 23, 214 
Simulinntspp, 61-62. 62 

Shusitis, 179, Sec also Chronic respiratory disease 

Skeletal system, 50, 50-51 


disorders of. 35. 56, 228 
and immunity, 44 
mites, 68, 69-71 
discoloration of, 159-160 
Slaked lime. 19 

Slipped tendon, 33, 35, 155, 226, 228, 229, 287. 303, 

Sod disease. Sec Ergotism 
Sodium, 193. Seealso Salt 
Soltinum spp, 142 
Sore head. See Pox 
Sorghum poisoning, 140, 155 
Sour crop. 160. 174 
Species specificity, 5 
Spirilla. 109, 709 

Spirochetosis. 39, 48,59,73, 110, 116, 196, 304-305 
and human health, 305 
postmortem findings, 175, 176, 177, 304 
symptoms of, 153. 155, 160, 162, 164, 304 

Split- wing syndrome. See Infectious stunting 

Index 343 

Spondylolisthesis. See Kinky back 
Spontaneous sex change, 54 
Spores, I0H, 129 
Sporozoites, 98, 104 
Sporulalion. 98 

Staphylococci, 109, 109. 188. 189. 190 
Staphylococcic arthritis, 110, 1 17, 155, 162,305, 

and human health, 231, 305 
Staphylococcic septicemia, 305 
Staphylococcosis, 110, 116-117. 188, 189, 190, 191, 

and human health, 231, 240, 243 
Staphylococcus aureus. 1 10, 238, 240 
Star-gazing, 227, 228. See also Epidemic tremor 
Starvation, 39, 225 
Sterilizer, 21 

Sternal bursitis. See Breast blister 
Steroids, 194 

Stomach worms. 85, 86-87 

Stomatitis. See Thrush 

Strep infection. See Streptococcosis 

Streptococci, 109, 109. 110, 188, 189 

Streptococcosis, 110, 117. 199,270,306 
postmortem findings. 175, 176,306 
symptoms or, 153. 155, 162, 163, 164,306 
treatment of. 188. 189, 190 

Streptococcus equisimilis. 1 17 

S.faecalis. See Omphalitis 

S. zooepulemicus. See Streptococcosis 

Stress, 3. 22 

behavior. 23-25 

and disease, 192, 223 

heat-. 28, 134-135, 136, 140 

and immunity, 199, 201 

and nutrition. 28,31, 32, 33, 193 

and shock, 194 
Stress disease. See Chronic respiratory disease 
Stroiwtoides avium. 85, 86-87 
Stunting syndrome. See Infectious stunting 

Subulura spp. 86-87 
Sudden death, 164 

Sudden death syndrome, 131, 154, 164, 175, 176, 

302, 306-307 
Sulfa drugs, 188, 189, 192 
Sulfonamides, 188, 189, 192 
Summer disease. See liluecomh 

as disinfectant. 21 

and fertility, 214 

and nutrition. 26, 29 
Supportive therapy, 192-194 
Surgery, 195 

Susceptibility. 12, 35,197 

Swollen head syndrome. 110. 131. 156, 158, 161, 


Symptoms, 148, 150-151, 152-164, 244. Seealso 

Syndrome, 131 

Synergism, 190 

Syn S amuslr U clw„.aR-B7.m 

Synovitis, 50-51, 179. Seeo/so Infectious synovitis 

Syringe, 185. 185 

Syringophilus bipemms, 68, 71 
Systemic diseases, 55. See also Septicemia 
Systemic inhibitors. 76 


Tapeworms. 62. 77, 711. 78-79, 79. 89-90, 90, 155 
Taxusspp. 142 

Temperature. See Body temperature. Heal, 

Incubation, Winter care 
Tenosynovitis. See Viral arthritis 
Terriiorialism, 25 
Tetracyclines. 189, 191 
Tetrameresspp. 85, 86-87 
Thermoactinoinyces vulgaris. 231, 233 
Thirst, 24, 32, 39 
Thorny-headed worm. 86-87, 88 
Thrush. 8, 39, 129, 130, 130. 308 

and human health. 130, 231 , 308 

resemblance to: canker, 256; crop impaction, 
264: Newcastle disease, 291 

symptoms of, 152, 160, 162, 163, 174, 308 
Tibial rotation. See Twisted leg 
Tick paralysis. 73, 155, 251, 287 
Ticks, 59, 68, 73. 73-74. 74. 1 16 

and human health, 74, 231, 234 
Tissue sampling. 178 
Toe-punching. 222-223. 223 
Toes, crooked. 226-227 
Topical drugs, 183 
Torticollis. See Wry neck 
Toxic fats. 39 

Toxicoinfection. See Botulism 

Toxic plants, 1 42 

Toxins. See Poisoning 

Toxoplasma gondii. See Toxoplasmosis 

Toxoplasmosis, 97, 106, 188,308-309 

and human health. 231, 235, 309 

symptoms of, 152. 154, 159, 161, 163, 176,308- 

Transmission of disease, 6. 6, U4-U5. 215, 2/6. 

Treatment of disease. 181-182, 195 

Trematodes. See Flukes 

Triatoma spp, 59 

Trichomonas gnllinae. See Canker 

Trichomoniasis. See Canker 

Trkhostrongulus tenuis. 86-87 

Tricholheecne mycotoxicosis. See Fusarioioxicosis 

Triple sulfa. 188 

Trombicula* spp, 68, 72,72 

Tuberculosis, 18, 18, 110, 1 17-1 18, 309-31(1 
and human health, 118.310 
postmortem findings. 174, 175, 176, 177,309 
resemblance to: lymphoid leukosis. 285; Maiek i 
disease, 287 

344 The Chicken Health Handbook 

Tuberculosis (conlimiett) 

symptoms of, 153, 156,159,309 

Tumors, 82, i is, 126-129, 128, 178. Steak® Lesions 

Twisted leg. 131, 154,303,310, 310 
l'vphoid.8,39, 110,115, 196, 199,215,311 
postmortem findings, 175, 176, 177.311 

cholera. 258: colibacillosis, 263; paraiyphold, 
294: pulloruni, 299; spirochetosis. 304 
symptoms of, 152, 158, 162, 163, 164.311 

Ulcerative enteritis. 8, 1 10. 1 1 1. 1 15. 31 1-312 
resemblance to: campylobacteriosis. 256; 
coccidiosis, 261: infectious anemia, 275; 
necrotic enteritis, 289 
symptoms of, 152, 164. 174. 175, 176, 177.312 
Urates. 48, 151. See also Cimit 
Urine salts, 48, 151. SeeahoCtwt 
Urolithiasis. See Gout (visceral) 
Uveitis. See Marek's disease 

Vaccination, 13, 197, 199, 202-206. 203 

failure. 121, 122, 200. 206-207 
Vaccine, 200-202 

Valgus deformation. See Twisted leg 

Valgus log deformity. See Twisted leg 

Varus deformation. See Twisted leg 

Vector, 6 

Vehicles, 5. 6-7 

Vent brush vaccination. 204 

Vent gleet. See Pasted vent 

Ventilation, 15-16, 62-63, 192 
and incubation, 210, 218-219 

Vent pasting, 152, 160, 295-296 

Vent picking, 53. 137 

Vesicular dermatitis. See Ergotism 

Vetch poisoning, 142 

Veterinarians, 167 

Veterinary ethology, 23 

Vibrionic hepatitis. SeeCampvlobacleriosis 

Wrfnspp, 142 

Viral arthritis, 121, 122, 154.201.205,215,305 313 
Viral diseases. 119. 120-121, 122. 186-187 
Viral enteritis, 123 
Viricide, 21 
Virulence, 22, 107 

Viruses, 15, 119, 120-121. 120-121, 122. 186, 199, 

See also Vaccine 
Visceral lymphoma. See Lymphoid leukosis 
Visceral urate deposition. See Gout (visceral) 
Vitamin A, 28-29, 30, 33. 34-35, .56. .80,214,217. 

227, 228,269.264 
Vitamin B. 30, 30-31. 35, 217, 227,228 
Vitamin C. 30,31 

Vitamin D. 29. 30, 31. 34-35. 157, 180, 217, 228 
V.tamin E, 29, 30, 34-35, 180, 214. 217, 227 228 
229. 269 

Vitamin K, 29,30, 34, 180, 188, 190,217,228,229 
Vitamins, 28-31,30,31,33,216 
Vitamin therapy. 193 
VVD, See Twisted Leg 


consumption. 39, 40,39-11, 135, 148 
deprivation. 40-41, 41. 48. 54, 156. 180. 193, 226 
and disease, 39, 42, 192 

23, 1 84. 184 

Water belly. See Broiler ascites 

Winter care 


White diarrhea. See Pullorum 

White muscle disease. 33, 154, 174,228,313-314 

Wild birds, 1 1 

Windpuff, 267 

Windswept. See Twisted leg 

Wing cot. See Necrotic dermatitis 

Wing-web vaccination, 204, 205 

Winter care, 41. 42. 33. 39, 132-133 

Withdrawal period, 82, 104, 191,237 

Wood floors, 14 

Wormers. 80. 80-82, 84 

Worms, 15. 22, 77, 79, 79-82, 87. 193 

detection of, 92-96 

and embryonation, 7ft 83 

and human health, 231, 235 

symptoms of. 79. 80. 87, 153, 160 

See also Capillary worms, Gapeworms, 
Roundworms, Tapeworms 
Wounds, 194 
Wryneck, 221 

Xandiomatosis, 39 

X disease. See Aflatoxicosis. Bluccomb 

Yew poisoning, 142 
YOgnrt, 193-194 
Yolk peritonitis. 53 

Yolk sac infection, 262. Seealso Omphalitis 

Zii* deficiency, 217, 228 
Zoonoses, 231, 235-237